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Biology 202, Spring 2005
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MK McGovern

Have you ever arrived at home or work with no memory of how you got there? When you started on your journey, you thought about the first few steps on that familiar path, but somewhere along the way, your brain moved onto more interesting topics, and the next thing you knew, you'd arrived. This is the essence of habits - once you start on a familiar series of actions, you stop thinking about them, and you are able to complete them without conscious thought or attention (3,4). This can be both a boon and a bane to humans as it frees up our minds from dull or repetitive tasks, but also makes it difficult to stop a habit once it's started. What differentiates the learning that forms habits from other types of learning? How do habits form? Why are habits so hard to break? How does the brain know which learned behaviors to translate into habits? What does this imply about our day-to-day behavior?

Habits are a series of steps learned gradually and sometimes without conscious awareness (2,3,4). Habit formation is a type of procedural learning in which the basal ganglia, a cluster of nuclei located in the forebrain between the cortex and the brainstem (1,11), play a key role (1,2,3). The location of the basal ganglia provides access to both the cognitive areas of the brain involved in decision making (forebrain) and also the midbrain which controls motor movement (1,11). It is the only place in the brain that deals with both physical and cognitive actions simultaneously, linking thought to movement (10). This linking occurs via projections from the basal ganglia into the thalamic nuclei (associated with the frontal cortex and cognitive functions) and the brainstem nuclei (associated with motor control) (1).

The area of the basal ganglia that has been particularly associated with habit formation is called the striatum. This area receives the most input from the cortex and may be involved in cortico-basal ganglia loops using the thalamic connections mentioned above. These loops may be involved in the decision to select certain actions, e.g. the automatized response of habits. In addition, the striatum receives input from dopamine-containing neurons in the midbrain or brainstem. Together, these inputs may create a loop with the striatum that leads to habit formation by associating rewards (dopamine) with a particular context (1,3).

In experiments involving rats with striatal neuron sensors, a restructuring of neural response patterns was indicated during habit formation. As a sequence of steps was learned, basal ganglia activity was present during all steps, but as training continued, this activity became centered around the beginning and end of the task. The dopamine-containing midbrain neurons shifted their firing pattern to respond to the earliest indicator of reward, e.g. the start of the habit task (3). Essentially, the dopamine-containing neurons fired predictively, which suggests the development of an action template in the striatum so the steps of a task are treated as one behavioral unit (1,3).

There are several possible mechanisms for the development of this action template: the gradual tuning of certain modules of striatal neurons, spatiotemporal binding by striatal neurons, and convergence of information on striatal targets (2). Although the exact mechanism remains unknown at this point, the coding of tasks into units or chunks is supported by behaviors like obsessive-compulsive disorder (OCD). The striatum of OCD patients shows consistent abnormal patterns of activity that abate with treatment. The symptoms of OCD involve sequential repetitive behaviors driven by extraordinary compulsions. These behaviors are performed as chunks and are directly linked to the striatum by the patterns of activity mentioned above (2). Additionally, after monkeys were trained in a three step task, the monkeys continued onto the third step even when the reward was given at the second step, indicating a chunking of the task. This chunking was linked to the striatum when pretraining damage to the monkey's striatum led it to stop at the second step instead. This indicated that damage to the striatum prevented the binding of the task into a unit as had been previously observed (2).

Chunking of tasks allows for the automated nature of habit behavior. In fact, attention to the tasks involved in a habit could lead to its disruption (2). This emphasizes the importance of slow learning in habits. This gradual development provides a selection mechanism for which task sequences will be encoded as habits. Only those tasks which are repeated over a period of time have the potential to become habits. This is particularly important since the predictive firing of dopamine-containing neurons and the chunking of habit steps makes it especially difficult to break a habit once it is formed (2).

Since a habit is a series of behaviors bound together and initiated by a particular context, avoiding this initiating step could be key to breaking a habit (8). Habits are formed by the repetition of a particular neural pathway leading to a reward. When a habit is being formed, learning creates a bombardment of action potentials that strongly depolarize a target cell so that fewer action potentials are need to trigger depolarization in the future. This can create a neural pathway - a series of connected neurons whose polarization is permanently raised closer to the threshold potential making it easier to propagate action potentials down this path. In order to break a habit, it might be necessary to prevent particular neural pathways from being selected (11). This could be done by creating new neural pathways that are preferred, i.e. making a new habit to take the place of the undesirable one (8).

The importance of the initiating step in performance of habits is underscored by certain behaviors associated with Parkinson's. Since the release of dopamine is associated with the beginning step of a habit, a lack of predictive capacity, i.e. the ability to anticipate a reward and release dopamine at the start of a habit chunk, could impair sensorimotor functionality (2). This would lead to behaviors similar to those displayed by Parkinson's patients, in which they have particular difficulty starting and stopping movement sequences, or switching from one sequence to another (3). The role of the basal ganglia in task switching is illustrated by a decrease in this ability by patients with basal ganglia damage. For example, patients with Huntington's disease made significantly more errors in selecting a sample item from a group of items which were identical to the sample along one dimension (6). This indicates a difficulty in switching attention between dimensions, thus linking the basal ganglia with the ability to readily switch between learned procedures or habits (6).

Once a habit chunk has been initiated, problems can occur if there are defects in the inhibitory influence of output neurons in the basal ganglia (4). Neuroimaging of patients with Tourette's Syndrome shows abnormal levels of activity in the striatum (1) indicating a connection between overactivity in the basal ganglia and tics (4,7). In fact, tics have been suggested as the building blocks of habits (4), so overactivity along habit pathways could lead to the uncontrolled tic behaviors characteristic of Tourette's.

The acquisition and performance of habits can also be manipulated by certain drugs. It is in fact this manipulation of the habit formation process that could be the underlying mechanism of addiction (9). For example, there is heightened activity in the striatum which is associated with a proportionate increase in stereotyped behavior when rats are treated with drugs such as cocaine or amphetamine (1). This heightened activity may act like a switch in the basal ganglia which changes a habit into an addiction (9). In addition, if a small surgical change is made in the addicted rat's basal ganglia, it loses its addiction immediately (7). Since even one dose of these drugs can be addictive, the gradual, repetitive nature of habit formation is circumvented, possibly due to a chemical change from the sudden, massive reward of a high (9).

The idea of the basal ganglia as a key player in habit formation is further strengthened by studies which dissociate other areas of the brain associated with learning and memory, e.g. the hippocampus and the amygdala, from habit formation. The hippocampus is involved in explicit, factual learning and memories (11). The amygdala maintains emotional memory (11). Experiments in which rats are given a choice between a cue response (striatal use) and a spatial response (hippocampus use) for a trained habit task follow along structural damage lines. That is, rats with hippocampus damage show a cue response and those with striatal damage show a spatial response. Similarly, rats were able to acquire habits with amygdala damage, but did not show acquisition of stimulus-reward information, and vice-versa with striatal damage. This pattern indicates parallel and simultaneous acquisition of the task during habit learning for the hippocampus, amygdala, and striatum along with a shift in strategy based on location of damage (5). Further, it indicates a dissociation of learning and memory functions among these structures (5).

Habits are differentiated from other types of learning both structurally (basal ganglia changes) and behaviorally (incrementally, unconsciously acquired). They are essentially discrete, quantized patterns of behavior that comprise major portions of individual everyday existence. The complexity of conscious behaviors requires the surrender of routine tasks to the unconscious in order to allow a basic level of multi-tasking. For example, habits allow us to walk around the block and talk to companion at the same time, to eat while we watch TV, to find our way home while dissecting the exam we just took in our mind. While this is certainly convenient in many ways, this surrender of control also leads to questions regarding free will. Can habits alter one's brain structure in such a way that free will is lost? Isn't this the essence of addictions? How is the conflict between one's conscious will and the unconscious force of habits reconciled?


Note that starred (*) sources are accessible only to Bryn Mawr, Haverford, and Swarthmore students through Tripod

1) Graybiel, Ann. (2000). "The Basal Ganglia." Current Biology, 10(14), R509-511.

2) Graybiel, Ann. (1998). "The Basal Ganglia and Chunking of Action Repertoires." Neurobiology of Learning and Memory, 70, 119-136.*

3) Jog, Mandar, Yasuo Kubota, Christopher Connolly, Viveka Hillegaart, and Ann Graybiel. (1999). "Building Neural Representations of Habits." Science, 286, 1745-1749.*

4) Leckman, James and Mark Riddle. (2000). "Tourette's Syndrome: When Habit-Forming Systems Form Habits of Their Own?" Neuron, 28, 349-354.*

5) McDonald, R.J. and N.S. Hong. (2004). "A Dissociation of Dorso-Lateral Striatum and Amygdala Function on the Same Stimulus-Response Habit Task." Neuroscience, 124, 507-513.*

6) Packard, Mark and Barbara Knowlton. (2002). "Learning and Memory Functions of the Basal Ganglia." Annual Review of Neuroscience, 25, 563-593.*

7) Anthony, Richard. (2001). "Changing Habits: Brain Studies May Help Us Overcome Destructive Behaviors." Spectrum, MIT, online.

8) Eveld, Edward. (2000). "It's Time to Break Those Bad Habits; Here's How." The Kansas City Star, online.

9) "The Infinite Mind: Habit." (2003). The Infinite Mind, online.

10) Halber, Deborah. (1999). "Work Probes Why Habits Are Hard to Make, Break." News Office, MIT, online.

11) Campbell, Neil and Jane Reece. (2002). Biology (Sixth Edition). San Francisco: Pearson Education, Inc.

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