Week 6 - Neurobiology and Behavior

Paul Grobstein's picture

And now we have central pattern generators and corollary dischage signals and .... Thoughts about those, and what we can/can't do with them to understand ... ? Or anything else that's been on your mind/brain this week.

JaymElaine's picture

Phantom Limb

So, this week I wanted to talk about phantom limb. I thought that this was actually cool to think about; surely such a condition is not cool to experience, but noneoftheless, I liked learning about it. Phantom limb is a condition in which a victim of a lost limb still feels that his/her limb still exists and that that limb can still feel sensation. See when one loses a limb, he/she is merely losing skin, some bone, a little muscle, and a few hundred nerve endings. But what is interesting is that the nerve beginnings are still in tact, and they still fire. These firings make the victim feel as though his/her limb is still there. Phantom limb can be quite painful, for nerves are firing and no output is being produced as a result; so what happens? More firing. And this leads to the brain being so fustrated with trying to tell the lost-limb a message that it causes pain for the victim.  Now that we know of this condition, let us not assume that people who complain about a lost limb are "crazy"; instead let us educate others who may not know about this neurological condition in hopes of providing more sympathy to those victims of phantom limb.

Jayme E. Hopkins, '08

emilie's picture

Corollary discharge signals and eye movement

I am currently taking a Visual Neuroscience class at UPenn and it has really opened my eyes (no pun intended) to the complexities of the nervous system, especially the visual system. There are so many intricacies to the vision that after 3 weeks of class, I couldn't even imagine how much more we were going to learn about vision because we had already covered so many things!

Anyway, to the point of this posting, I read a study that discussed the importance of corollary discharge signals in saccadic eye movement, which are the rapid, voluntary shifts in eye position between steady fixations. In this study, they recorded from certain corollary discharge signal neurons in a primate model. The recorded from neurons that were known to relay between the superior colliculus (an important visual center in the brain) to the frontal eye field. They then injected a certain chemical to inhibit the relay system and in turn found that the primates were no longer able to make saccadic movments between two fixed points and that the second saccade was completely off from the first saccade. So, what this demonstrates is that corollary discharge signals are important in mainting a steady visual precept despite sudden retinal shifts caused by saccades.

kgins's picture

less wrong

Less on neurobiology specific, more on the story telling way of "getting it less wrong"... I was thinking about stories- how they're as "good" to us as useful as we can make of them... how we build off of them, and potentially go a "less wrong" place each time.  I think part of the reason why we'll never be "right"- why there can't really be an absolute- is because of these stories, and because we're the interpretters.  We're the ones who design the stories- maybe not the actions or the thing we're telling a story about, but the words, and method of story telling. I think that stories are as useful to you as they are in the present moment, and just that. I think experience makes us want to believe- or find more useful, things that we may not have considered before a certain point, and I think that makes us biased, and by that, we can't judge a story simply for the story, but for what it lends us- whatever comfort, explanation, anything, it gives us.  I think that we look to these stories to inspire us- to make us think, to make us understand a little better, so that we can come up with more questions, more possibilities. I think that with this, our biased minds will find useful what they will as a result of how we've come to be who we are, and by that, no story can ever really be "right", unless it's purely by chance, by randomness- something we may never know.

Kathleen Myers's picture

Predicting Intentions

I just read an article in the science section of the NTY that I found very provocative and disturbing- "Scientists Try to Predict Intentions".

The story is this: scientists at Berlin's Bernstein Center for Computational Neuroscience have been studying the MRIs of people engaged in making decisions- at this stage of research the decisions are simple ones- whether to add or subtract two numbers, or which of two buttons to push. These neuroscientists were able to determine that the brain activity associated with decision-making is mostly localized to the prefrontal cortex region; further, by studying the MRI images associated with different intentions ("I will subtract" or "I will push the red button" they were able to identify what they called "thought signatures", patterns associated with addition, subtraction, etc. They claim to have "identified people's decisions about how they would later do a high-level mental activity".

At this point, their predictive accuracy rate is 71%, which is only 20% better than pure chance, but still, what astounding consequences this could have on our somewhat fragile civil liberties. Are the "thought police" far behind? In Britain, the article said, the powers-that-be are already keeping track of  known malcontents (who have not yet committed any crime)as potential future criminals. Throw in some really invasive technology that can identify intentions and you've got a sci-fi situation on your hands. Or a situation from our collective past- the witch trials of Europe or the McCarthy hearings in the US. Just add MRIs! Frightening stuff.

But, to be fair, the article also points out the fact that such resesearch and the technologies it may engender could proved enormpusly helpful for paralyzed people.

Shayna or Sheness Israel's picture

Well, Social Science Does This ALL The Time...

What was interesting, for me , in reading Myers post about natural scientist predicting intent is that social scientist--particularly sociologists--attempt to create (sociological/methodological) tools to predict and prescribe intent all the time. However, the difference is that natural scientist have better operationalized and standardized tools that make the results intersubjectively knowable--objective.

Is this the fear: natural scientist have better tools for predicting intent that can almost be used by and for anyone?

If so, I could see that as a valid point. Yet, I would bet that there will always be a percentage left that represents the intent that cannot be predicted. That minute percentage would account for all variation. And that is no small issue.

Sasha's picture

Treating motion sickness

After reading numerous postings on motion sickness I began to wonder how we prevent it. Dramamine (dimenhydrinate) an oral medication and Transderm Scop (scopolamine) a patch you place behind your ear are perhaps the two most widely prescribed treatments. Having previous experience with both drugs I never realized they actually worked by crossing the blood brain barrier and acted in the central nervous system. After last weeks lecture it seems incredibly obvious now that the most logical place to send inhibitors would be the brain. Scopolamine (in Transderm Scop) works by inhibiting the secretion of saliva and sweat and decreasing gastrointestinal secretions and motility. More directly- the medicine works by reducing the activity of nerve fibers in our inner ear- which is as we discussed in class what brings about the discrepancy between the sensory discharge and the corollary discharge. Unfortunately from reading through the pharmacology of this medication I couldn’t distinguish between whether or not the drug is acting on one particular system-such as the sensory discharge- because it is directly reducing the movement in our ear, or if it is working on both sensory and corollary because it is effecting the entire system? Regardless, it is amazing that chemical inhibitors are able to have what seems to be pretty direct control over various inputs and expectations. With that in mind, perhaps I am missing something in the complete understanding of how the drug is working, but if we are able to develop a drug that is inhibiting one type of mismatch between sensory discharge and corollary discharge, then why can’t something similar be developed to control the sensations of phantom limb?Drug Info: http://www.rxlist.com/cgi/generic/transscop_cp.htm

AnnaM's picture

While I was at lecture last

While I was at lecture last Thursday, learning about corollary discharges and the discomfort that occurs when signals from sensory and inter neurons disagree, my friend was fast asleep in my room. He had not intended to spend a night in Bryn Mawr, but his sleep cycle prevented him from even being alert enough to navigate public transit home. He has a combination of two different conditions that affect the body's internal clock, or circadian rhythm: Delayed Sleep Phase Syndrome (DSPS) and Non 24-hour Sleep-Wake Syndrome.


Delayed sleep phase syndrome means being physically unable to fall asleep until very late hours at night, and unable to wake up until late morning or afternoon. This would be fine if all jobs and classes were flexible enough to accomodate all sleep schedules, but the U.S. generally runs on a 9-5 schedule, which may be impossible to keep for a person with DSPS. Also, people with "normal" circadian rhythm patterns can compensate for a lack of sleep the night before by going to bed earlier the next night, thus "resetting" the internal clock. A person with DSPS may not be able to sleep until whatever their "normal" bedtime is, even if they are sleep deprived. (See wikipedia's entry on dsps for more info).

Non-24 hour sleep-wake syndrome is a more serious condition, in which the person's brain and body insist that the day is longer than 24 hours. In practice, this amounts to gradual delays in sleeping and waking time over the course of days, until the person's "clock" has finally run its cycle. (This cycle, when left unchecked, is known as free running). Again, this cycle doesn't work particularly well in a world that demands 9-5 work or class in most cases.(See wikipedia's article on non 24-hour sleep-wake syndrome for more info).


So where do central pattern generators and corollary discharges fit into this picture? Given the explanation of motion sickness last Thursday, it seems to me that you could probably apply a similar model to circadian rhythm disorders. In DSPS and Non 24-Hour Sleep-Wake syndrome, the central pattern generators in the body, probably in combination with hormones from the endocrine system (like melatonin), register the feeling of tiredness during daylight hours. But their sensory neurons register sunlight, light sky, people moving-all obvious signs of day, a time when one shouldn't be asleep. Maybe the disconnect between these inputs is one factor that makes circadian rhythm disorders so difficult to manage.

Also: Not ever country runs on a 9-5 clock like the US does. In a country where keeping later hours is the norm, would a person be diagnosed with DSPS if, say, they went to bed at 11 and woke up at 7 or 8, a time frame that would be considered typical or desirable in the US? The disconnects between inputs would be fundamentally the same, but the desirable time frame varies so much. Does DSPS even exist as a diagnosis in other parts of the world?

Molly Tamulevich's picture


When we discussed why we throw up when we feel a non-localized interruption of our corollary discharge, I started thinking about how ridiculous it is. I mean, the notion that our body's raction to unknown stress is sleep made me laugh. I had never thought about it like that before. I wonder, though, if it is the same with depression. One of the main symptoms of depression is an increase or disruption of sleep activities. Is it possible that the stress of the chemical imbalance or situation that provokes depressive episodes interferes with our corollary discharge in a way that parallels non-localized stress such as motion sickness? Do mental inputs have the same kind of painful effect on the body as physical ones?

Liz S's picture

somatic symptoms

I agree with Antonia - mental inputs such as depression can most ceretainly have the physical effects on the body. In the case of depression, there are a whole host of physical symptoms - lack of appetite, fatigue, increase or decrease in sleep patterns, etc. that the DSM lists as criteria for an episode of major depression.

Also, children represent depression with more physical symptoms. This may be because they lack the words to explain mental anguish, but in other countries depression is also seen as a more somatic illness. Yes, there are cultural differences in what's an accepted disorder/way of feeling/norm, but I believe that mental inputs can most definitely lead to painful (or the opposite) effects on the body.

And just to note, anxiety presents with a lot of somatic symptoms (and anxiety is most certainly tied in with stress).

Antonia J's picture

Stress and Depression

In response to Molly's last question, I think that mental inputs most certainly can have huge effects on the body, both positive and negative. It has also been recently proven that the incidence of depression increases with the number of important life events that have occurred. It seems that stress and depression are strongly linked in some way. Whether stress causes depression, or whether it is merely the stimulus that a certain chemical predisposition needs to develop the disorder, I don't know. I'm not quite sure how this ties in with our corollary discharge, though... I do agree, however, with michelle, that the benefits of corollary discharge signals outweigh the negative effects.

I also am starting to think, like Michelle, that behavior is not regulated by "consciousness" as I now think of it. Perhaps all we really are are machines, and we have no real control over our destiny. It's an unnerving thought, and I don't believe it... but this class is certainly making me think about this kind of stuff....

alexa09's picture

conscious vs. unconscious

I think I wrote about this briefly before, but, according to an article in the New York Times, “Free Will: Now You Have It, Now You Don't”, we are like machines in that most of what we think to be conscious decisions are unconscious. According to the article the conscious brain only plays catch-up to what the unconscious brain has already done. The decision to act is an illusion that you make about something that your unconscious has decided.

In some ways I believe humans are very ignorant about what goes on in the body and in the mind. We really don’t know how and why we decide to do things. Granted the conscious mind can give logical reasons for doing things but why does one “choose” to do that action? If it isn’t our decision then how does our unconscious decide what to do?

At a children’s fair, a clown approached a little boy and blew on a flat balloon and then presented the balloon to the child. The child looked at the clown blankly and the clown repeated his action. The child still did not understand so the clown approached me with the same act. I blew on the balloon and it became inflated. I had no idea when and why I made the decision to blow on the balloon. Why did my unconscious mind decide that I should blow on the balloon? Why did the unconscious mind of the boy react the same way?

michelle's picture

Letting Our Nervous System Do Its Thang

Before taking this class, I was a strong advocate of taking responsibility for one’s actions. I believed humans were ultimately in control of their behavior (excluding patients who are mentally ill due to chemical imbalances, etc). Now, I’m starting to think differently, especially after learning about corollary discharge signals and central pattern generators. Our perceptions of our inputs are now jaded by corollary discharge signals and our movements can be performed without conscious thinking due to central pattern generators. I’m starting to think that after taking this course, I’m going to ultimately come to the conclusion that our own conscious thinking has very little to do with our behavior.

I also started wondering how these corollary discharge signals and central pattern generators are important in terms of evolution and life. I remember watching this discovery channel episode about the brain, where there was this study done to test participants ability to walk over hurdles (somewhat like an easy obstacle course) while listening to random words. At the end of the obstacle course, they were asked to recite the words said to them. Older patients remembered few to no words while younger patients remembered most of the words. The scientist concluded that older patients needed more of their brain to concentrate on walking and therefore could not concentrate on remembering the words. Younger patients were better at multitasking. That’s scary to think that as people age, their central pattern generators don’t function as well, and therefore repetitive tasks like walking require conscious thinking in order to perform.

This study exemplified how essential it is to be able to perform more than one task at a time as well as how important it is for our corollary discharge signals to monitor our inputs. Without such devices, we wouldn’t be able to sip coffee while reading, read while on the elliptical, see an unshaken world, etc. The benefits definitely outweigh the trivial costs of motion sickness.

After reading the post on autogenic feedback training, I began to think how dangerous such device could be. Maybe we are not in control of such autonomous nervous system functions for a reason. Maybe our nervous system knows what’s best for us. Tampering with the way our body is supposed to function always seems wrong to me because the body is so perfectly designed for a reason. That’s why I hate taking drugs (even Advil), because I believe that most of the time, our bodies are perfectly capable of dealing with its own problems. And most of the problems we face with our bodies are due to us not taking care of our bodies. I don’t’ know…. Just some thoughts.

dmckeever's picture

Free Will?

I am growing equally worried that free will doesn't truly exist. My entire life, I have been told that I make my own choices and I am responsible for how I  live my life, but just as the above post said, if these patterns intrinsic to our bodies really do exist, then it seems we have much less control over the inputs and ouputs of life  than we thought. The post “Predicting Intentions” got me thinking: scientists have identified patterns of thinking and decision-making for their subjects—are these specific to that person? Are they a result of the structure of the brain and other parts of the nervous system? The implication is that whatever is the source of these patterns somewhat (if not completely) dictates our thinking, which is where I thought our free will began, and our decision-making, which is where I was under the impression our free will manifested itself. If this is not the case, the new have no free will? If how we think is dictated by the physical structure of our brain, then we never truly have an original, personal thought? So then, can anyone be  responsible for their thoughts and actions? Can fanatics that hold racist and  prejudicial beliefs, and then act on them, be held accountable? This has dangerous implications. We  operate on the impression that we are in control of ourselves and our environment; what if these scientists could predict, say, a presidential candidate’s decision about war just by looking  at his/her MRI? Would we begin voting based on brain patterns and not political parties and views? And, that choice I made yesterday, if it wasn’t really a voluntary choice, what does that mean? Then, who are we really? I think that this says something about the human race: we are not as superior as we like to believe; we are just animals acting on  instinct and being driven by our inner workings, much like animals of the wild, with whom we do not associate ourselves. We are more like them then we’d  like to believe.

jpena's picture

Who are we?

I was also struggling with the concept of free will. I learned about reward pathways in the brain when writing my web paper. They are pathways that create the desire in our brain to repeat behaviors that stimulate the pathway and give us a feeling of pleasure. Even eating triggers a reward pathway. In my paper I focused on addiction and how reward pathways cause us to loose some of our free will. It also made me think about the simple activities that our brain almost tells us to do without our conscious thought. This idea makes me wonder who we are. Am I just a product of my brain? If this is the case then it seems like I am not even an autonomous individual. I am willing to accept the idea that the mind can be in total control of the body but I want to believe that I can also identify with my body. This is becoming increasingly difficult to do as I progress through this course.

Holly Stewart's picture

Intrinsic Harmony

It still somewhat boggles my mind there are these central pattern generators that act the way they do. I was thinking about the swimmerets as well as our own human function and I am still trying to work it all out.

I enjoy the idea of thinking of our system as a symphony; and I don’t even mind that there is not one specific central conductor of the symphony. But what is still confusing me is the fact that although everyone is playing different scores of music, everything is flowing perfectly together. The first chair violin player is not only playing independently, but also communicating via distant hand signals across the pit with the obo first chair and is still able to explain exactly what is going on. The system is maintaining intrinsic harmony. For me, this is my new definition for homeostasis.

This lack of control is still a bit mind-boggling to me. I am not satisfied to think the system is only communicating via nervous and endocrine signals – there must be more to it than that. How is it that the swimmerets are able to not only work together but able to work independently? Why is it that we seem to have such difficulty in locating a central pattern generator? Are the outputs of central pattern generators weighed? This last question seems quite pertinent for expanding on what we already know. If central pattern generators are everywhere throughout the system, and they are constantly communicating then things are definitely getting busy! But do these central pattern generators able to assess the validity of what the other central pattern generators are saying? An example: the swimmerets are moving in a specific pattern, yet this doesn’t mean the lobster is unable to move its antennae. So how do the central pattern generators communicate? How do they evaluate the importance of what another central pattern generator is doing? I have so many more questions!

I recognize these central pattern generators help to support the I-Function box, but I am still a bit unconvinced. These systems are all about communication, yet I don’t see the kind of communication coming out of the I-Function Box that I would expect. Could the I-Function Box be a central pattern generator itself? I think it may in fact be. It dictates control over a specific system, yet remains in communication with all other systems. Maybe the I-Function Box is the central pattern generator for the brain. I still have more thinking to do about all this…

LS's picture

Did I just say that out loud?!?!?

  I was online looking for example of disorders associated with corollary discharge other than just car sickness and.  I actually found a couple of article and a student web paper from 2003 (http://serendip.brynmawr.edu/bb/neuro/neuro03/web2/mcoleman.html) that were on corollary discharge and schizophrenia.  From what I have been able to gather corollary discharge comes into play with individuals who have positive schizophrenic symptoms particularly auditory hallucinations.  Apparently for individuals with schizophrenia their corollary discharge does not work properly and they have trouble distinguishing covert speech, thoughts, from overt speech, things that are actually said.  I have never really though about it until this point but it would be really difficult and scary if you could not determine your thoughts from what you were actually saying!  Imagine thinking something terrible about a friend’s new hair cut and not realizing whether you were thinking it or actually saying it!

I think, further, this may have implications (as posted earlier) for perception.  If your corollary discharge is not working property there are huge implications on many levels.  Also, humans are all very different so I wonder if there are minute differences in our corollary discharge that actually cause us to experiences things different, not having as large an implication as in schizophrenia but still having an effect….just more to ponder…and to be thankful that as far as I know my corollary discharge is just fine, thank god!

Lauren Poon's picture


When I look back at last Thursday’s notes, the central pattern generator’s interest factor seems disappointing compared to other matters covered in class. For one, the CPG feels more tangible in principle than do other aspects of the brain like the I function or the mind.

I was searching for research and found a lot of robotic work pertaining to the CPG. Robotic movements are primarily governed by mathematical patterns to imitate those conducted by the CPG. Once study used a nonlinear oscillator equation to control the robot’s gait. The robot’s CPG mimic that of an organic being such that the output was unaffected by outside conditions, and had fast transitions because movement is steady. After reviewing this study and many others, I find the CPG to be fairly comprehensive in the fact that its principles can be easily generated in mechanics and physics. I don’t feel like the subject is debatable or controversial.

I was also thinking about evolution and its effect on CPG. CPG control automatic movements like walking. Evolution suggests man went from walking on all fours to walking on two legs. Surely, the CPG had to adjust as man changed its gait. How do innate patterns change in brain?


eden's picture

I’m not flighty, I’m just corollarily challenged

So I was thinking about what we were discussing in class; that we can walk without thinking about it, type on a computer without consciously sending a signal to each finger at each moment, etc. I thought this was very interesting, and I happily continued to peruse the issue in my head. I thought about motion sickness and mixed signals, and about the blood vessels in your eyes that you don’t “see” even though they are there… I was merrily meditating on all these ideas, when suddenly I looked down and realized I had been taking notes on organic chemistry the entire time. I didn’t remember a lick of the stuff I was writing, but there it was, on the page. It was even legible and coherent. I found this rather amusing and startlingly appropriate.

Someone mentioned in one of their posts how they sometimes correlated personality with how the aforementioned phenomena might affect different people. Now, to be honest, I kinda feel that with all this talk about everything being “a product of the brain” and i-boxes within boxes and whatnot, our definition of personality has probs been mangled beyond recognition at this point, however, if I were able to send myself back to the time before I was enrolled in this class, back when things were simple, I would have said to you that I have a very “scatter-brained” personality. I am the queen of tangents. I am the empress of non sequiturs. I think nine things at once, and when I try to say them all they get garbled together and it comes out all wrong and is therefore usually interpreted as dirty(as most things are). A former boyfriend of mine was always complaining that I would be in the middle of a conversation with him and suddenly I would run away and start talking to someone else. When he would confront me about it later, I’d just get confused because I couldn’t remember that I hadn’t finished our conversation before I ran off and started the next one. My point is, I always wondered what the heck was wrong with me that new thoughts were always flooding into my head and I couldn’t freaking concentrate on one thing, that I could move on to something new without even realizing it. I guess what I am trying to say is that like walking, or typing, or taking notes while thinking about something else, the human brain seems to apply this concept of ignoring certain signals and focusing on others to everything, not just physical stimuli but “I-function” type (self perpetuated) stimuli too. I think that’s pretty sweet.

That being said, I think my “I-function” regulator is broken.

Maybe that’s what I’ll use as my excuse next time my friend yells at me because my room is a mess. I mean seriously, do you know how hard it is to clean your room with a busted corollary discharge monitor? Not easy my friends, not easy.

Claire Ceriani's picture

Carsickness and Driving

I know someone who gets very carsick, even in the front seat, but only as a passenger.  As a driver, she's fine.  This makes me wonder what the difference is.  Though you really spend the majority of your time looking forward (rather than out the side window) while driving, there is still the sensation that the world is moving around you, yet the brain doesn't seem to have a problem with this.  Your eyes must also take in moving images from the rearview mirror, the side mirrors, and the side window, plus the stationary images of the speedometer, fuel gauge, etc.  Why doesn't the brain have a problem with all of these conflicting inputs?  Perhaps the very action of driving seems more like moving than just going along for the ride.  By taking an active part in actually driving the car, you feel more as if you are moving through the world, rather than sitting in a stationary car as the world flashes by the window.

Sarah Powers's picture

Tabula rasa--Not in neural development

I read the short paper linked to the outline of our lecture which basically says that even people born without limbs--not just amputees--have phantom limb syndrome. This implies that we are born with an internal neural map.  So the neurons in the central nervous system that lead out to a hand that was either amputated or never there to begin with 'expect to see' a hand, but they just end at the stump of the limb, which causes the discordance and discomfort.  The important part is that the neurons have this expectation even without amputation. Think about the theory of tabula rasa--when we are born our minds are a clean slate. We know our brains are made out of neurons, like the neurons that go from our central nervous systems out to our hands.  If there is a map for the patterning of neurons from the central nervous system to the hand, wouldn't it follow that there is a map for the neurons in our brains?  Not really a clean slate, is it? There would have to be, considering we are born knowing how to breath, knowing when we're hungry--both processes are mediated by the brain.  But how far does this map extend into the brain? How much is there a map for? If there's a map for a hand that doesn't even exist, is there a map in the brain for connections that still are to be made? These might be questions more appropriate for a developmental biologist, but it's still interesting to consider the extent of our internal neural map.

biophile's picture

The emerging mind

I'm familiar with the concept of a system without a director, but it seems strange to think of the brain without a center of activity (or, rather, to think of it as not being the center of activity for the body). As someone posted earlier, where does this leave the I function? It makes sense to me that certain parts of the nervous system coordinate to perform certain functions without the guidance of a conductor, as in the swimmeret example. I can see how this would work in many contexts, but what about higher brain functions? It seems as if there would be a driving force behind consciousness instead of the mere coordination of different functions. Again, it makes sense that unconscious workings would involve separate functions working together... It just seems bizarre to apply that model to the I-function. We don't usually experience ourselves as being split into many different processes coordinating to achieve a certain end. Most people experience themselves as whole and cohesive, even though some parts of themselves remain a mystery. This whole ramble is probably off the mark, but I've been wondering how our sense of selves can be accounted for in this model of neural systems. It's especially mind-boggling now that we're mentioning things that have been talked about in my emergence class... On some intuitive level the connection between emergence and neurobiology are is there, but it's so hard to articulate (especially when human thought is thrown into the mix).

Meera Seth's picture

A Chaotic Brain

According to a new study conducted by German scientists at the University of Bonn and published in the online edition of the Nature Neuroscience journal, the brain appears to function and process data more chaotically than previously believed. These researchers claim that the standard model in which information is received and transferred from neuron to neuron does not only occur at the synapses. This study suggests that neurons release chemical messengers along the full length of the extensions, thereby stimulating the neighboring cells.

More specifically, the researchers studied the "white matter" in rats' brains. This part of the brain holds the linkages between the left and right halves. These links are comprised of axons and ancillary cells, however notably lack dendrites and synapses. This implies that one would not expect to witness the release of messengers in this area of the brain. However, the scientists were capable of showing that certain cells in the white matter react to glutamate, a key neurotransmitter which is released when signals are found at synapses.

If correct, this groundbreaking discovery not only shatters widely validated findings about the brain and its fundamental mechanisms, but could also potentially lead to the development of new drug therapies.

x's picture

Chubby Babies = Overweight Kids?

I read this article on CNN Health: (http://www.cnn.com/2007/HEALTH/parenting/03/05/weight.puberty.reut/index.html)

It very briefly states the main points of a recent finding that girls who are overweight toddlers (around age 3) are more likely to start puberty earlier and become overweight adolescents.

"Earlier onset of puberty in girls has been associated with a number of adverse outcomes, including psychiatric disorders and deficits in psychosocial functioning, earlier initiation of alcohol use, sexual intercourse and teenage pregnancy and increased rates of adult obesity and reproductive cancers," the study claims.

What is it about the combination of brain chemicals and a higher BMI that causes these psychological side effects? I am skeptical of this study simply because it gives no details as to how it was conducted, who conducted it, and what the original hypothesis was. I am also interested in why they chose only girls to study. Is there a different psychological weight phenomenon occuring with boys? If so, what, and why?

Darlene Forde's picture

Can Central Pattern Generators be successfully reproduced?

I found the concept of central pattern generators (CPG) and corollary discharge sequences intriguing. They offer a means of understanding the nervous system in intriguing ways that reflect both the complexity of interactions associated with specific types of response, and the simplicity inherent in the physical manifestation of these responses. Yet I wonder how easily specific patterns can be fully identified and sequenced. In class we considered how such systems might operate within simple sea creatures. Using such methods to understand behaviors in humans however, is (and will be) exceedingly more difficult. (We are unlikely to remove body parts of people in order to identify patterns within the CPG.)

Artificial life, however, offers a means by which we can learn and speculate about CPG in different life forms. Researchers at the University of Hawaii, for example, are working on developing robots and other forms of artificial intelligence by modeling the neuromorphic pattern generator of their robots after the CPG in humans. Indeed, they have implemented the use of what they call a “very large scale integrated (VLSI) chip” containing oscillator circuits designed to mimic the output of motor neurons in a way that parallels the actions of the CPG with its inherent simplicity in the physical manifestation of the response. The result is that the robots designed by these researchers walk more “smoothly” with less of the ungainly awkwardness associated with the walking gait control of robots.

Link to NIH

Pleiades's picture

Autogenic feedback training (AFT)

So I too have been thinking a lot about motion sickness lately. I’ve got a few friends who suffer a ridiculous amount when we sail, where I have never been sick (knock on teak). I was initially interested in what kind of personality correlated with who gets sick and who doesn’t, however all the information predicted I would get sick because it is generally the obsessive/anal people who are the ones that fall ill. So I continued without faith, and found something called autogenic feedback training, which is used frequently by NASA to help prevent their astronauts from getting space motion sickness. It is also used for people suffering from migraine or tension headaches to control peripheral blood flow and reduce forehead and/or trapezius muscle tension and training cancer patients to reduce the nauseagenic effects of chemotherapy. As far as I can tell, the patient is hooked up to bodily monitoring devises and basically watches them is able to control otherwise autonomic bodily functions (I couldn’t find a great definition I think because the method is patented). Studies show FTE subjects reported fewer or no symptoms at higher rotational velocities than subjects in the control or promethazine groups. The primary physiological effect of promethazine was an inhibition of skin conductance level. The AFTE group showed significantly less heart rate and skin conductance variability during motion sickness tests administered after training. So basically AFT is your I-function telling your autonomic systems (normally outside the I-box) what to do, and its better at it than drugs! So back to personalities, I think that people who have good control over there bodies and who can make their I-function tell there bodies not to get sick are the ones who don’t fall ill.

So perhaps the explanation about riding rollercoasters and not getting ill is that since you think you should enjoy the motion, it doesnt register as wrong and your I-function is able to controll the rest of your body. Personally I very much enjoy the up and down motion of a boat. Along this note, haveing crewed on a ship where we take landlubbers out to sea, we were told NEVER warn people about sea sickness. EVER. The more they think they are likely to get it, the more likely it will become that you will be cleaning up there puke (which is no fun).

A.Kyan's picture

More on AFT

I was also reading about NASA's approach to motion sickness.  (http://www.nasaexplores.com/show2_k_4a.php?id=01-040&gl=k4)  I told Tommy (my boyfriend) that my theory on overcoming motion sickness has some basis and that he should try it so he can go on rides with me!  I love rollercoasters and anything that spins.  Although, I can handle rough rides, I am subjected to motion sickness while I read in the car or on a boat- (even though planes are okay).  When the feelings of fatigue and queasiness arise, I concentrate on those sensations and the symptoms pass without discomfort.  However, I haven't been able to manage to focus on the sick feelings and read at the same time, so reading in cars/boats are still out for me, although I no longer feel motion sickness otherwise. 

The articles states that it's "mind over matter" and motion sickness can be alleviated via AFT better than pharmacological methods.  I am a believer that we have more control over our bodies than we think is possible.  For instance, if I'm going to the beach or on vacation, or simply don't want my period because I have an event to go to and it's that time of the month, I can delay my period by just not wanting it.  Then, as soon as the trip/event is over, I get my period immediately.  It works every time, and I love my body for coorperating!  How does this fit in with central pattern generators?  It looks like something else can influence the way our cpg works...        

A.Kyan's picture

More on AFT

I was also reading about NASA's approach to motion sickness.  (http://www.nasaexplores.com/show2_k_4a.php?id=01-040&gl=k4)  I told Tommy (my boyfriend) that my theory on overcoming motion sickness has some basis and that he should try it so he can go on rides with me!  I love rollercoasters and anything that spins.  Although, I can handle rough rides, I am subjected to motion sickness while I read in the car or on a boat- (even though planes are okay).  When the feelings of fatigue and queasiness arise, I concentrate on those sensations and the symptoms pass without discomfort.  However, I haven't been able to manage to focus on the sick feelings and read at the same time, so reading in cars/boats are still out for me, although I no longer feel motion sickness otherwise. 

The articles states that it's "mind over matter" and motion sickness can be alleviated via AFT better than pharmacological methods.  I am a believer that we have more control over our bodies than we think is possible.  For instance, if I'm going to the beach or on vacation, or simply don't want my period because I have an event to go to and it's that time of the month, I can delay my period by just not wanting it.  Then, as soon as the trip/event is over, I get my period immediately.  It works every time, and I love my body for coorperating!  How does this fit in with central pattern generators?  It looks like something else can influence the way our cpg works...        

Rebecca Pisciotta's picture

Integral Integration

I think one of the dangers of study in any field is becoming too narrowly focused on any one idea, and losing the grand integrative scope of things. This is not a critique, but a reminder I guess, something that we should always keep in mind. Neural control of body and brain is a huge part of the picture, but cannot be the whole picture. A central pattern generator may seemingly give us the ability to walk without thinking about it, but if our muscles did not have acetylcholine receptors we would not be able to move at all.

The mechanism of a central pattern generator is great for explaining how we can do things like walk without thinking about it, or (if we were birds) fly without learning how to. The mechanism of a CPG is not responsible for all the aspects of motor control though. Located along our muscles there are nerves with special receptors called stretch receptors, they respond to the stretching of one muscle that occurs when its antagonistic muscle contracts. The impulse elicited is neurally transmitted in a big circle (bypassing "conscious" control) and returns to the muscle in which it originated, and it causes the muscle to contract. This explains why we can spontaneously contract our knee and instead of getting stuck that way, it bounces out again. Because the muscle is contracted with a force proportional to the force with which it was stretched it also accounts for why we dont kick our doctor in the stomache when he does the pataellar tendon reflex test.

I think it would be inefficent of the brain to generate two patterns for each action, one for muscle (a) and one for muscle (b) the antagonistic muscle, or for it to generate a pattern that is twice as long because it specifies all contractions of muscles (a) and (b). It seems most efficent for our brain to take advantage of the role of reflexive motor mechanisms. Also if it does the latter it can utilize the contribution of gravity to the movement in order to expend less energy. So, for our brain to get its job done most efficently, it may utilize mechanisms and forces not under its direct control.

urbrainondrugs's picture

Could your arm be stuck upwards?


A central pattern generator is a collection of neurons that causes rhythmic movements in living creatures. They are motor symphonies that create oscillations or rhythmic activity independent of sensory inputs. Normally these neurons oscillate on their own and/or oscillate (fire) as the result of a cascading action potential going down a network of neurons. These were the two models we looked into during class. I was interested to know whether or not there are patterns of neurons where they cannot fire and cause a motor symphony alone, even if there is an outside stimulus to begin the action potential cascade. These neurons cannot work alone, but rather, will only function if they collect together and fire at the similar times. Are there certain patterns that require there to be a certain number of neurons to be present in the action and will only activate once there is a sufficient amount working together?

In the case of a biological being central pattern generator can send bursts down to activate a motor neuron which can cause a certain muscle to contract. However the muscle must also move back the other direction because the motor neuron is only responsible for this particular movement, so consequently there must be another central pattern generator system to create an opposing movement. Would your arm muscles contract if there was not a network of neurons present in order to contract the opposite direction and bring your arm back down? Also the models we looked at seemed to be continuous excitatory systems. Are these systems managed by a negative feedback loop so for example a muscle is not over stimulated? Is your nervous system aware whether or not there are neurons present to balance movements?

Cheers (a motor symphony with glasses)

Cayla McNally's picture

Flaws in Stem Cell Research

I came across an article in the New York Times, “Panel Finds Flawed Data in a Major Stem Cell Report”, that could possibly change the way people feel about stem cell research. In the past few years, there has been much arguing back and forth between people in the scientific, political, and religious worlds about research on stem cells, which were believed to be able to mature into any cell that a body needed. The problem that they could mainly come from aborted fetuses, but the benefit was that diseases such as Parkinson’s and Alzheimer’s would become things of the past. However, this article states that there are problems in the data that presented that stem cells could become any other cell in the body; those who have done the same experiments have come up with entirely different data, and the information is being reviewed by other scientists to see if it is still credible. While it is still uncertain whether or not the information is still viable, there is now a possibility that the high expectations that the both the scientific society and society as a whole had are incapable of being met.


francescamarangell's picture

Identifying Faces

I began reading articles on the internet about car sickness and the body’s natural response, when I came across an interesting yet unrelated article about faces and how the mind registers faces. It is believed that there is a special region of the brain that is specifically correlated to face recognition. This theory was presented when a man who had experienced a stroke showed difficulties identifying faces. A test was conducted where monkeys were shown regular objects, such as a banana or a book and their brains were monitored with fMRI. Then the monkeys were presented with images of faces, and their brains were again monitored. The highlighted regions of the brain were very clear. When a face was presented versus when a non face was presented, a specific region of the brain showed activation. Furthermore, when ordinary objects such as a shell or a tissue were configured in such ways that a face could be identified within a non-face that same region of the brain was activated but on a lesser level. Faces are an image that we see and interact with frequently. The image of a face, and the characteristics of a face are remembered within our brains, so when a non-face exhibits specific face-like patterns, our brain is able to identify those patterns as a face.

Ian Morton's picture

I think I read an article on

I think I read an article on the same study.


Cool beans.

alexandra mnuskin's picture

corollary discharge, I-function and the self

Like most of the others in the class I too was fascinated with the idea of corollary discharge. I frequently suffer carsickness…especially when I read. On the train and plane however I’m usually fine. I wonder why that is since the mixed messages from ones sensory inputs and corollary discharge are still present in any moving vehicle.
On a related note, I am still very confused about the I-functions role in all this. Is it like the example with Christopher Reeves…that his I-function has no play in his knee jerks? Are things corollary discharges something that we are not actually aware of…something that goes on inside without our thinking about and experiencing it? We discussed in class how the nervous system is really just a bunch of semi-autonomous parts coordinated by the interactions among them. That there is no conductor…no main central part that is really in charge. I can’t deny that I found this idea more and more disturbing the more I thought about it. I confess I’ve always believed, perhaps subconsciously, that there was some unifying force, soul, I function, in short--the self that which qualifies you as a thinking and reasoning human being. Is that not what the I-function is? How many of these semi-autonomous parts have to malfunction for you to be considered damaged or even dead? It seems that there is no longer that distinct line between life or death, sanity and insanity.

kjusewiczh's picture

Remembering the Motions

In my intro bio class this year we had a bolg on muscle memory. When we had that blog I never really though about what was behind muscle memory, I was just trying to finish my post so I would credit. Now that I'm in neurobio, though, I find myself thinking about what is behind muscle memory. I think that it is very clear that we use muscle memory every single day. We don't think about how to walk, talk, or write. Does msucle memory completely cut out the brain and just rely on the motor neurons connected to the muscles in question or is it happening so fast that we just do not realize that our brain is being used?

I have read stories when a man with complete amnesia can still "remember" how to play the piano as well as he could before. This man can also still walk and talk. If this man can't remember anything else and has brain damage, why can he do these things? Is that part of his brain working fine or is it just not a part of these activities?

Another issue this brings up in my mind is when people totally forget how to do something. When I was young I forget how to talk. I couldnt form words anymore. Was my brain taking over and trying to control my muscles? Or were my muscles just not reacting to stimuli in the correct way? I'm sure every single person has tripped while walking. Maybe nothing at all was in your way, but suddenly your leg didnt move in the right way and you stumbled. This could be a momentary laspse in your muscles memory or could your brain just be handling too much and just forgets to tell your leg to move. I think that muscle memory is a very interesting topic that contains many questions, at least for me.

eshuster's picture

This class is confusing

I am a third year biology major at BMC that has been shopping this class since my spring semester of my first year. Both my freshman and sophomore year I went to the first week of this class and decided not take it because I felt intimidated. Why should someone read my writing every week or my papers for the class? I had never taken a web based class before and was intimidated by that idea. Also, I heard (through people) that you will either love or hate this class. I couldn’t decide whether I would like it or hate it and the fear of hating the class made me choose a less risky class for that semester. As this is my last year at BMC I decided to try it out. It wouldn’t matter how well I would do in the class because I already have plans for next year, it would be a class for myself to see if I loved it or if I hated it. I also wasn’t sure I liked the idea that anyone could read my writing because it’s something I’m not confident in, since it isn’t my first language. I had many reasons to take this class, for the experience, and many reasons to avoid this class, because it may have been too different from what I was comfortable with.

Now that I have attended class and experienced the web emphasis I find that I’m challenging myself and my previous understanding of science. I am questioning what I know and what I am currently being taught. I don’t know how or why I come out of class confused but I know that I am trying to think about what is said in class and what I felt like I knew. Was I taught to think the wrong thing, through simplification? Did I interpret my previous understanding of neurons and the nervous system improperly what I originally learned it? How could almost everything I have always thought I new about the nervous system seem to be negated by one class? It’s as though this class is my class to be wrong in, something students try so hard not to do because we are afraid that our grade will suffer.

 I have always thought that the brain was the “central hub” of the nervous system and that the neurons must send signals through the spinal chord. Now I see that organisms have central generators that are not located at or near the brain. They act on each other and not through a central hub of information. I have seen that we can experience phantom limbs that we think are there but it’s because the nerves think that they are there. I was so confused in class this past week because my brain couldn’t wrap around the fact that we can feel what is not there. How can this be? Why don’t our nerves realize what has been lost? If we think it is there why can’t we start regenerating it?

Another aspect of this class that I like is that, I can be wrong without worrying about my grade. It’s the first time that it’s ok to be wrong. We have always been taught that we should learn from our mistakes but if we make a mistake on a test we can learn from it but our grade will suffer. This class is like the opposite. We have to be wrong in order to find the right answer and without being wrong we cannot do well because we then cannot find the right answer.

Overall, I’m really glad I took this risk and I think it came at a good time. I don’t know how I would have felt about this class if I took it earlier or later but it feels right or maybe it feels right because I can be wrong. This is my interpretation of the first half of the class I don’t know how I will feel in the second half but being wrong has never felt so right.  

RachelBrady's picture

Central Pattern Generator and Neuromodulatio

A central pattern generator is network of neurons found in the nervous system which is responsible for the generation of rhythmic behaviors such as walking, swimming, and breathing. This “motor symphony” of movement is not orchestrated by one unit, or conductor, but is the result of interaction between many semi-autonomous parts. Therefore, with CPG, an organism is able to exhibit rhythmic activity in the absence of sensory inputs. In class we discussed the development of CPGs as being genetic and/or the result of experience. CPGs are formed during early embryonic development where neuronal circuits are organized to enable spinal cord and brain stem circuits to generate efficient motor patterns, such as breathing. An illustration of the genetic origin of CPGs comes from the experiment discussed in class where new born birds where placed in straight jackets. After the period where a bird would normally ‘learn’ to fly had passed, the jackets where removed and the young birds were still able to fly.  This study indicates that the motor patterns necessary for flight are not learned. In order to further prove the genetic origin theory of CPGs it would be necessary to locate and change the specific gene and observe if the pattern changes (the motor patterns in flight, for example).  

What intrigues me is the idea that CPGs may be a result of experience and that these systems are modulated by sensory feedback. If CPGs induce natural rhythmic behaviors can the frequency and phases of a CPG be selectively modified to increase the accuracy and efficiency of a particular behavior? In searching for the answer to this question I came across an article by Paul S. Katz, David J. Fickbohm and Christina P. Lynn-Bullock. The article physiologically and morphologically identified specific neurons in opisthobranch mollusks shown to be part of the central pattern generator underlying dorsal swimming. They refer to these neurons as the dorsal swim interneurons, or DSIs.

The motor pattern for swimming is generated as a result of the properties of CPG neurons and their synaptic interconnections. Sensory neurons, which are located in the fused cerebropleural ganglion, synapse directly and indirectly on the dorsal ramp interneuron which monosynaptically excites the CPG dorsal swim interneurons. The DSIs synapse onto two other CPG interneuron types: cerebral neuron 2 (C2) and the ventral swim interneurons (VSIs).

The DISs are immunoreactive for the neurotransmitter serotonin. “Physiological evidence strongly suggests that the DSIs release serotonin and that it is used both as a classical neurotransmitter, evoking fast and slow synaptic actions, and as a neuromodulator, altering the cellular and synaptic properties of other neurons”. The effects of this modulation include the enhancement of synaptic strength and increased excitability of CPG cerebral interneuron 2.

When the DISs are active they evoke neuromodulatory actions on other CPG neurons modulating their cellular and synaptic properties. It would then be logical to assume that by naturally or artificially modifying DISs activity the resulting behavioral pattern of swimming can be changed, or enhanced.

What are some natural neuromodulators that affect central pattern generated behaviors in humans and can these be artificially modified in order to enhance behaviors? I’ll keep looking.



RachelBrady's picture

Neuromodulators are

Neuromodulators are neurotransmitter-like substances, delivered by the bloodstream or more rapidly via synaptic terminals, that enhance or diminish the effect of the primary neurotransmitters in nerve terminals. These substances alter the functional properties of neuron circuits by facilitating, depressing, or initiating motor activity as well as by modifying the cellular and synaptic characteristics of neurons. Within CPG networks, neuromodulators are classified as intrinsic (being an integral part of the CPG) or extrinsic (modulating CPG activity from other areas of the nervous system). Neurotransmitters (glutamate, GABA, glycine), as well as the neuromodulators (serotonin, dopamine), have been shown to influence locomotor CPG behavior. In addition, certain peptides have neuromodulatory effects on the locomotor CPGs.

Inconclusive studies have been conducted which measured improvements in mobility and EMG activity induced by treadmill training. What remains unclear is the relative contribution of plastic changes in neural pathways versus changes in the circuitry of CPGs. It has been argued that part of the training effect is due to strengthening of the lower-extremity muscles, although little evidence of a strengthening effect has been reported. Better understanding of neuromodulators on CPG activity and interlimb coordination; and the nature of mechanisms that seem to be prohibiting spinal locomotion in humans are practical importance. Locomotor CPGs may be manipulated to improve the quality of movement, and thus quality of life, for people with movement dysfunction.

lrifkin's picture

Motion Sickness

Class discussion this week peaked my interest in motion sickness. Although I myself generally do not experience any type of motion sickness, I have family and friends who do. I have watched curiously as they have needed to sit in the front of a bus, open a window, or get out of a moving vehicle completely.

This week I read an article about Dr. Stephen Hawking, who has studied gravity and plans to experience a world without it in the near future. Dr. Hawking had plans to go into space. However, first, he has plans to participate in a space flight simulation of sorts.

The company that provides these simulation experiences is called Zero Gravity Corporation and has been taking “thrill seekers” on this specific ride since 2004 for $3,500 a trip. However, the company was founded in 1993 and since then has entertained about 2,500 customers. What interested me about the Zero Gravity Corporation, and about their trips, is the fact that since their first trip only 1 or 2 percent of their clients have become “spacesick.” This means that despite being nicknamed the “vomit comet,” relatively few people experience motion sickness on these flight simulations.

Although I can understand motion sickness on land and on the sea, I am confused by motion sickness and space travel. In class we discussed the fact that astronauts usually feel extreme motion sickness within the first few hours after take off. After those first few hours the motion sickness generally subsides and the astronauts are able to comfortably work, explore, and relax. When in this simulator, and when in a spaceship, individuals are obviously unable to view any movement. However, are they able to sense movement in any other way? Does gravity affect the way in which human beings sense movement, or do not sense movement? Does a lack of gravity eventually eliminate any disagreement between the sensory input and the corollary discharge signals sent to an individual’s brain that could cause motion sickness? Why are astronauts only get “spacesick” during the first few hours of flight?

Sarah Harding's picture

Motion sickness without visual input?

I read the same article about Stephen Hawking's planned flight experience. What's interesting to me, is the fact that spacesickness can be experienced in a place where there is no visual input. I could be wrong, but I was under the impression that the vomit comet was a plane completely lined with padding on the inside. With that in mind, there should be no windows or any way for the passengers to see outside. So how does the motion sickness occur? In space sickness, isn't the nausea caused by a discrepancy between the inner ear and the visual input? If there is no visual input, there can be no discrepancy with the inner ear. Does motion sickness actually have nothing to do with your visuals, and more to do with the lack of gravity on your inner ear? To me, there should be no sensory-motor conflict if you are unable to see what's going on. Someone mentioned in class that if you have poor vision, your chances of getting motion sick were slimmer. What if you are blind, can you never get motion sick? If so, this should be the same as the window-less cabin...

That brings me to a few other questions: If your inner ear is damaged, can you a) experience motion sickness? b) function at all?

Jessica Wurtz's picture

More on Motion Sickness

This subject intrigued me as well. I used to be able to read in the car, but now I prefer to sleep through a long car trip; I don't get really ill, just sort of headachey. My sister however, gets sick unless she is driving or sitting in the front seat so she can't see the world go by the side window. However, she does not get sick at all on roller coasters or other motion sick rides. I would think that the more extreme motion of a theme park ride would make her more sick than a car trip. I'm sure there are actual physiological and neuronal reasons for this, like that you're moving so fast on a ride, maybe you can't really see things go by clear enough to get sick (much like the people with bad vision on a boat we talked about in class). But I also wonder if it has anything to do with the context of the motion sickness potential. A five hour car drive where you know you're going to get sick feeling is not as much fun as a 2 minute thrill ride. I thought maybe it was the difference in time spent in motion, but if you spin around fast for 2 minutes either on your feet or on a merry-go-round, it is likely to make you much more ill than the roller coaster. So what makes it different? At least for those things you're still on the ground, as opposed to being flipped upside down and backwards 50 feet in the air.  What makes the nervous system confused about one and not the other? And why do you have the same sense of the world spinning when you spin around whether or not you do it with your eyes open or closed, I would think that would make a difference, since the confusion is based on conflicting sensory input. Why does the nervous system have to be so confusing is what it comes down to I guess.

secaldwe's picture

Oops, there goes my lunch...

I have suffered from violent motion sickness for all of my life. I can’t read in the car, I can’t read on a train and as I learned this past summer, I CANNOT deal with life on a cruise ship. (Oh well, I’ll never be a sea captain…) As discussed in class, puking is the nervous system’s generalized response when it can’t locate the source of a problem. But why? Why do we barf automatically? Jessica mentioned simply feeling a headache. I get that too, but mine is always accompanied by a rising gorge, followed by a car rapidly pulling over or better yet, me ralphing into one of those wax-lined “barf bags” from airplanes. Does the throbbing behind the temples trigger said automated response? I took this opportunity to look up “vomit” in various online journals and learned that the sensation known as nausea does not always lead to forceful expulsion of one’s stomach contents. In fact, we vomit mostly due to increase ICP (intracranial pressure). Who knew?


Receptors in the medulla are the source of the unpleasant sensation. Though we are not entirely sure which neurotransmitters actually regulate vomiting, we know that some prescription drugs reduce the risk by inhibiting dopamine, serotonin and histamine. None of this, however, explains Jessica’s fascinating query about thrill rides. My father pukes after any loopy roller coasters. I could ride them for hours on end. Quick story: while vacationing at Universal Studios, FL, ride operators allowed me and a friend to remain on the Mummy ride (a backwards roller coaster in the dark with strobe lights) for five consecutive runs without getting off because we were cute and had these fast passes from our on-site hotel. I didn’t once feel a wave of nausea, even though I had consumed a funnel cake and perhaps an alcoholic beverage or two not twenty minutes prior to this experience. What gives? I am at a loss. I’m sure if I tried to read on the ride, I would have tossed my cookies but just plain getting on an airplane makes me want to wretch. Is that similar to the space shuttle? Is pressurized air a factor?

csandrinic's picture

mute screaming

This week’s discussion about corollary discharge was very intriguing to me. From what I understand, corollary discharge signaling is the phenomenon of the brain sending a signal to various muscles to create an output and a copy of the signal getting sent to the auditory system, desensitizing it so it doesn’t get overloaded. I read a very interesting article in the New York Times called “Block that Chirp: Volume Control in Crickets”. (http://www.nytimes.com/2006/01/31/science/31obox.html?ex=1173157200&en=d1f5c958d1946aec&ei=5070) In crickets, it has been determined that at the precise moment a cricket moves its forewing muscles to create a chirp, its auditory neurons become inhibited. However, no corollary signal is created when the cricket moves the same muscles- albeit in a different pattern- while flying. It can therefore be assumed that at the same time that the central nervous system sends a signal to the motor nerves, it also produces a corollary discharge that inhibits the response of the auditory neurons. This is of course the response in someone or something that has proper functioning of all of their body parts. But what happens when you have corollary discharge in a person who does not have this proper functioning? If you are mute, and you pretend to scream, will there be a signal that gets sent to your auditory neurons? Will they desensitize themselves even though you are not capable of making any noise? Is this like phantom limb, where an expectation signal is being sent out to the limb, even though the input signal is not present? Do mutes experience discomfort in the part of their body that expects to receive a signal but doesn’t in the same way that an armless person will experience discomfort in the area where their limb should be?

Alex Hansen's picture

I was also equally intrigued

I was also equally intrigued by this week's discussion on corollary discharge.  However, I thought about it in a different sense, which still can be applied to these crickets, for it is more of an overall take or question on corollary discharge.  I thought about it more in the terms of evolution and wondering how this nervous system trait came about.  Has is always existed since the beginning of time?  Has corollary discharge evolved over time?  Why has it evolved, that is if it has evolved and did not always occur?  Will the nervous system slowly evolve until corollary discharge is the only manner in which to look at the system, corollary discharge overpowers any other type of signaling?  Is there a connection between the types of animals that exhibit this corollary discharge?  If so what is the similarity, besides the fact that they share this nervous system trait?  They say that nervous systems differ from the others in two ways, one being their degree of centralization, and the other in their size.  Could this eventually become another explantion for the divergence in nervous systems?  Are there any other types of divergences that are to come?

Is corollary discharge evolutionary advantageous?  In that, is corollary discharge something that has evolved due to survival of the fittest, and that it produced the most advantageous results for the animal and thus, corollary discharge came to power.  This is also known as evolution by natural selection - survival arises from what leads to the most reproductive success, and thus, and therefore, whatever is most successful will inturn be passed along to the next generation, ultimately leading to the survival of that successful attribute.  From pyschology I learned about moose and the size of their horns and how their horns evolved by natural selection as the fittest survived and that trait was passed along to their offspring, passed off to the next generation.  I'm sure there are many more examples of this, and maybe the same is happening with the auditory systems in crickets with relation to the corollary system.  Could this be possible at all?

Ian Morton's picture

cricket singing

I thought I would make this a reply since I examined another article on corollary discharge in crickets.

As we have learned in class, proprioceptors continually update our nervous system with sensory information on changes in the body, constituting part of the “reafferent loop” of our nervous system.  However, there is a risk that these internally generated signals may become confused with sensory information from external stimuli, or they may desensitize an animal’s sensory pathways.  In order to prevent this, corollary discharges are sent to sensory regions and tell the nervous system to ignore the self-generated sensory feedback.  This is similar to the activity in which we watched our fingers move but noticed no movement in the background.  Corollary discharge influences and fine-tunes how we interpret sensory information.

The question, then, is what cells mediate this activity?  Through studying crickets, James Poulet and Berthold Hedwig have found a single type of interneuron is responsible for the pre- and postsynaptic inhibition of the auditory sensory neurons in crickets when they sing (1).  Why crickets?  Crickets hear with their forelegs and generate song with their wings, and the whole time while singing, they are fully sensitive to auditory input (1).  There must then be some neurons along the prioprioceptive and auditory pathways that mediate the inputs received by the CNS during song production that allow the cricket to maintain full sensitivity to auditory input, and this is accomplished with corollary discharge.

The cell responsible is known as a corollary discharge interneuron, CDI.  Poulet and Hedwig outline three major structural properties of CDIs that allow them to operate as they do.  First, the cell body/dendrites are located in the mesothoracic ganglion, which allows the cell to receive input from the singing CPG.  Second, the axonal branching overlaps with the auditory neuropil (gray matter) in the prothoracic ganglion in such a way so as to allow for direct synaptic output to auditory neurons.  Third, the axon also extends to various are of the CNS and could therefore affect the other sensory pathways involved with singing.

It was observed that the CDIs would fire synchronously with wing-closing motor activity (song production) and auditory inhibition.  I won’t discuss the experiments, but the results suggest that CDIs are both necessary and sufficient for mediation of corollary discharge during singing.  If you’d like more detail, a link to the article is provided below.

I just thought this article was interesting as it gives some beginning insight to the molecular basis of corollary discharge.  The article was from January of 2006, and I imagine there is still much to learn about the cells acting behind corollary discharge.

1. http://www.sciencemag.org/cgi/content/full/311/5760/518

katherine's picture

Mal de Debarquement

Stacy’s post that mentioned mal de debarquement syndrome made me curious about this condition.  After getting off a boat, many people feel like they are still rocking on a boat temporarily, but in rare cases, the condition can last for months of even years.  I came across a story in the BBC about a woman who has been suffering from mdds for four years!  She has tried a variety of treatments and even contacted experts in the field for advice, but nothing has been successful. 

Stacy wondered if anyone had any ideas about what may cause this condition, but I am completely baffled.  It seems logical that immediately after you got off of a boat you might still feel like you were rocking because your system has gotten used to the sensation and has synchronized itself with the rocking motion; when you get off, it takes time for your body to adjust to its new surroundings.  What really confuses me is that this condition can last for months or years.  Given that some people recover from this condition relatively quickly and others, like the woman in the article, never recover it seems that some people suffer some sort of permanent change.  But what is it?  For people that experience mdds for just a few months and then recover, why?  What accounts for these differences?

Aditya's picture

     Things like

     Things like watching my finger move, and expecting images in the background to remain still are things I have always taken for granted. It's absolutely amazing how our brain can provide the complex function of keeping an image still as it moves across the retina through the interaction of corollary discharge signals.  But also, this brings up the point that the reality we perceive depends on if our corollary discharge signal are in effect, or how they are interacting. Corollary discharge signals might be interacting differently in different people and thus different people might interpret the same reality in different ways. Thus, a stampede of questions comes into mind.

 Is this part of  the explanation for individuality? Does this contribute to why we are all different from each other? Is it possible that we each may have different central pattern generators that generate patterns for the interaction of corollary discharge signals? Could this explain why people have different unique walks, different enough from another person to verify your identity?


Could this explain why our enjoyment of types of music varies from person to person? Why some have more rhythym than others? Does trying to explain these individual differences with central pattern generators and patterns of corollary discharge signals seem too farfetched?

We are all equipped with  generally the same brains, with the same parts and connections, capable of the same functions yet we are all so different with regard to personalities, skills and talents, and preferences. I personally think the variability of central pattern generators and how corollary discharge signals interact in each person might explain this.

James Damascus's picture

Corrolary Discharge, Gait and Musical Preference

I really thought this was interesting article on motion capture technology, which is directly related to our discussion of corollary discharge and central pattern generators. I wonder, though, just how much of our unique gaits are affected by conscious choice and learned patterns of behavior (for example, youths walking a certain way in urban areas or models walking down runways). If in fact our walking patterns can be changed to fool pattern recognition software, would return to our "set point" walking style once we stop consciously manipulating our strides? If so, is this controlled solely by corollary discharge?

Although brain activity has been monitored while listening to music, and different types of music can produce different sensations (experiences) in different listeners, I don't think the specific pathways for different musical variations (sounds or patterns of sounds) are known to the extent that we could label this aspect of individuality a byproduct of corollary discharge. I think the best we can do at this point is suggest that there is a physiological (material) basis to "musical taste" and that variation between individuals' neuronal arrangement is responsible in some part for differences in musical preference (there are different kinds of feelings-ex. elation-provoked by different types of music). Clearly, no two people can have the same experience (no two nervous systems are identical),. Further, if Emily Dickenson is right, then all aspects of individuality originate from some difference in neuroanatomy.

Stacy Blecher's picture

It was interesting to

It was interesting to discover the cause of motion sickness.  Now, not only can I explain to people experiencing motion sickness what exactly is going on to produce these symptoms, but I can also offer helpful tips on how to alleviate the discomfort.  I also feel that I have a much better understanding of the phantom limb phenomenon, because prior to class I was one of those people who would just assume an amputee complaining of limb pain was crazy.   However, while I understand that the basic underlying cause of motion sickness is that there is a disagreement between the sensory input and the corollary input that the brain is receiving, a few questions remain. 

People generally experience motion sickness only when they take long trips in the car.   This makes sense because there is some sort of threshold amount of disagreement that the brain can handle before it freaks out and makes you vomit and go to sleep.  The medications that are typically prescribed to people complaining of motion sickness are drugs that inhibit the input of sensory information.  Valium is a drug that is occasionally prescribed for the treatment of motion sickness.  Taking valium before a long car trip causes one to fall asleep, thereby cutting off all visual input.  Essentially, taking medication just cuts out the middle step (vomiting) of the process ones body would naturally go through.  Yet, even when one is asleep the brain is receiving lots of sensory inputs.  When the car windows are down does ones skin feel the wind blowing past and interpret it as an affect of you moving?  If so, then even if ones eyes are closed, cutting out the visual input that says “you are moving”, the brain will still be getting the message “hey, you’re moving!” but it will be coming from sensory receptors in the skin instead of the eye.  This makes me wonder if there is some kind of hierarchy in the nervous systems.  That is, do sensory inputs originating in the eyes have greater influence on the brain than inputs coming from the skin?

This question also came up in the discussion about phantom limb pain.  If one receives a corollary signal from the neurons of the amputated limb warning the brain to expect pain, but all of the sensory receptors are reporting that there is no limb in which to feel pain, then why don’t the sensory signals correct the corollary signal?  Do the corollary signals hold more sway over the brain than the sensory signals?

            Something that completely stumped me was the condition known as "mal de debarquement."  This is when one feels perfectly fine on a boat at high sea but becomes nauseous and disoriented on steady, dry land.  Can anyone think of an explanation for this?