This paper reflects the research and thoughts of a student at the time the paper was written for a course at Bryn Mawr College. Like other materials on Serendip, it is not intended to be "authoritative" but rather to help others further develop their own explorations. Web links were active as of the time the paper was posted but are not updated.
2004 Second Web Paper
One of the most visible ways alcohol affects an individual is the loss of inhibitions observed in those with blood alcohol levels as low as .01% (1). Every college student has experience with the behavioral effects of alcohol. Friends become more outgoing and appear to lose all inhibitions as they continue to drink. A normally shy individual may be table dancing or a quiet friend may be the center of attention. This paper will explore the possible causes of this outgoing and sometimes outrageous behavior as well as the reasoning behind the consumption of alcohol beyond an individual's limit that occurs during drinking.
The prefrontal cortex, located at the anterior end of the frontal lobes, is specifically responsible for normal control of impulses. The prefrontal cortex has been linked to impulse control because damage to this region of the brain can lead to loss of inhibitions (2). One particular example of prefrontal cortex damage is the injury suffered by Phineas Gage. Gage had a steel rod penetrate his brain. He survived the incident but had poor impulse control over his actions that had not been part of his personality before the injury (5).
Individuals who consume alcohol can show impulsive and reckless behavior similar to those with frontal lobe damage. Since the frontal lobes have been previously linked to impulse control through studying individuals like Gage, I hypothesize that alcohol may act on these same regions to cause a loss of inhibitions. Additional evidence that alcohol acts on the frontal lobes was discovered when chronic alcoholism was linked to structural and neurophysiologic abnormalities that can be observed on functional magnetic resonance imaging scans (8). Ethanol must be working on the frontal lobes in order to inflict this damage over time. Further study of ethanol's effects on the frontal lobes led to alcohol's specific interactions with two neurotransmitters.
Neurotransmitters are released into a synaptic cleft between neurons and can cause an excitatory or inhibitory response. An excitatory response is produced when a neurotransmitter from the pre-synaptic neuron causes the depolarization and release of a neurotransmitter from the post-synaptic neuron (3). An inhibitory response is caused when the pre-synaptic neurotransmitter inhibits the release of a post-synaptic neurotransmitter (3).
Two neurotransmitters, gamma-amino butyric acid (GABA) and dopamine are responsible for the loss of impulse control in those who consume alcohol. Dopamine causes an excitatory response at dopamine receptors in the frontal lobes (7). Alcohol increases the amount of dopamine acting on receptors and enhances the normal feeling of pleasure associated with the dopamine system (7). Alcohol may function like cigarette smoke to inhibit the action of enzyme monoamine oxidase, the enzyme responsible for breaking down dopamine in the synaptic cleft (7). Since dopamine is not broken down as efficiently when ethanol is present, it can act on the post-synaptic neuron for a longer period of time. The feeling of pleasure will be increased and the individual will want to keep drinking to maintain the sensation. Individuals want to continue to experience the feelings caused by dopamine, so they continue to consume alcohol. The response of ordering another drink when one is already visibly intoxicated can be explained by the pleasurable effect that an increased alcohol concentration has on the brain.
Alcohol also enhances the effects of the neurotransmitter GABA on GABA receptors in the prefrontal cortex (4). GABA neurotransmitters inhibit the release of other neurotransmitters from post-synaptic neurons. Ethanol co-binds with GABA neurotransmitters to GABA receptors on chloride ion channels (6). Ethanol causes the prolonged opening of the chloride ion channels and the greater uptake of chloride ions by the post-synaptic cell. The presence of chloride ions hyperpolarizes the post-synaptic neuron so it cannot conduct an action potential and initiate a response to stimulus (6). Since the post-synaptic neuron cannot release a signal, the ability of the neurons in the frontal lobes to inhibit socially unacceptable behavior is reduced. Decision-making is also impaired and the impulsive, uncontrolled behavior of intoxicated individuals results. Dr. Richard Olsen conducted research on specific GABA receptors. GABA receptors with beta-3-detla subunits remain open for an extended period of time when exposed to low levels of alcohol (1). This particular subunit probably has a higher affinity for the binding of ethanol. GABA receptors Dr. Olsen studied respond to much lower levels than GABA receptors with gamma-2 subunits and nervous system control over behavior can be altered after one drink (1). The varying binding site shapes of GABA receptors may explain the progressive loss of control that alcohol causes. Some receptors respond to lower levels of ethanol and as alcohol concentrations increase more GABA receptors are affected. The loss of inhibitions results because the post-synaptic neurons are progressively less able to conduct an action potential and illicit a response.
The effect of alcohol on the GABA and dopamine systems causes the loss of control that can be observed when individuals drink. Through excitatory and inhibitory synapses, the actions of certain neurotransmitters alter the behavior of an intoxicated individual. Further study of the specific binding of ethanol to receptors may lead to treatment of intoxicated individuals. Also, studying the effects of alcohol will lead to a greater understanding of the role GABA and dopamine neurotransmitters play in altering observable human behavior. .
1)Even a little alcohol Affects the Brain, This online article written by Steven Reinberg contains a summary of the Research done by Dr. Richard Olsen on various GABA receptors.
2)Executive Functions and Frontal Cortex, This is a website containing information on the function of the frontal lobes and specifically the prefrontal cortex.
3)Synapses, This article provides good background information on the structure and function of neurons as well as a description of excitatory and inhibitory responses.
4) Neural Activity and GABA/Glutamate in Prefrontal Cortex: A Combined fMRI/MRS-Study, This site states that GABA does function in the prefrontal cortex. It wants to study the specific amounts of GABA in individuals using fMRI technology.
5)The Story of Phineas Gage, This is the story of Phineas Gage, including his background and specifics about his injury.
6) How Drugs Affect Neurotransmitters, This site provides text and a diagram about the affects of GABA on a post-synaptic neuron.
7) Tobacco, Alcohol and Dopamine, This site discusses the many impacts that alcohol and tobacco have on the brain, including their effects on the dopamine system.
8) FRONTAL LOBE CHANGES IN ALCOHOLISM: A REVIEW OF THE LITERATURE, This site presents research data from those who studied the effects of alcoholism on the frontal lobes.
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