Chronic alcoholism leads to down-regulation of a patient's GABAergic system and/or up-regulation of the patient's glutaminergic neurotransmission. In other words, in the case of the GABA system, chronic alcohol abuse will (since alcohol works as a GABA agonist) necessitate the administration of a GABA agonist. In the case of glutaminergic neurotransmission, chronic alcohol abuse will lead to an up-regulation of the NMDA receptor system (since alcohol is also an NMDA receptor antagonist).
Impact of drinking on information processing capacity in college-aged students
Sensory information processing in college aged students is impacted with frequency of consumption of alcohol. In the figure at left, frequency of consumption, in terms of drinks per month, is plotted against an adaptation metric. This demonstrates that this metric is sensitive to subtle changes in centrally mediated information processing. The more someone in this age group drinks, the higher the probability that there will be an impact on brain health.
It is widely known that alcoholics often suffer from peripheral neuropathy, a condition that results in a decrease in sensitivity or increase in thresholds. However, in the group of college-aged students that were studied, there was no evidence of this condition.
People suffering from chronic alcoholism also have reduced reaction times – another characteristic not shared by the subjects in this study. The absence of loss of function in either reaction time or sensitivity ascribes to the resolving power of the metric: changes in central information processing were detected although changes in metrics that are predominantly peripherally mediated were not.
Impact of acute alcohol consumption on the CNS.
Acute alcohol consumption in healthy controls (n=5) causes a shift in adaptation metrics. Consider the graph to the left: With blood alcohol (BAC) readings between 0-0.4, there is a significant difference between the pre-conditioning and post-conditioning measure (no adapt vs. adapt). However, after the BAC increases (0.5-0.9; red) in the same subjects, there is a significant decrease in the difference between the adaptation metric.
Impact of chronic alcohol consumption.
The CNS regulates itself to tolerate all sorts of abuse. Long term alcohol consumption will lead to the brain to changing its neurotransmitter levels to compensate for the effects of alcohol. In other words, an alcoholic will appear “normal” when he/she is at a certain level of non-sobriety. Thus, when the alcoholic becomes sober, he/she may have problems with excitability (seizures, etc.). Adaptation measures, which depend on the overall balance of excitation/inhibition in the brain, will reflect this.
Group comparisons of healthy adults with adults with alcoholism (Pilot data, n=12) demonstrates significant differences in the CNS alterations that occur both with and without an adapting stimulus (data at left). Before treatment, which was primarily a 12 week period of sobriety with behavioral intervention, subjects’ values appeared very different from those of controls. Note that after treatment, the values of the alcohol subjects appear to be much more similar to control values.
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