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inhibitory or excitatory) and determine the specific behavior of the receptor. There are four NTs important with reference to alcohol effect and dependence, the excitatory NT glutamate, the inhibitory NT GABA (gamma- aminobutyric acid) & the two NTs involved in the reward process: Dopamine and serotonin.
In initial exposure, alcohol induces production of dopamine, which onsets the encoding of these incidences as environment linked memories in cortex of brain. It also influences the excitatory and inhibitory NTs which in absence of alcohol, maintain a balance. Under the influence of alcohol,
an important subset of glutamate (N-methyl D-aspartate, NMDA) is inhibited, thus causing inhibition of excitatory impulse.The primary effect of alcohol, however is on NT GABA: its inhibitory effect is enhanced, resulting in suppresing neuronal activity of receptor cell. Here one of the key features of brain comes into play, that is adaptation. Adaptation in the same system, i.e. homologous adaptation results with repeated exposure to alcohol, and thus a tolerance is developed, GABA receptors become less responsive to GABA and higher alcohol concentrations are required to achieve the same level of suppression.
Upon withdrawl of alcohol, GABA receptors still remain less responsive and hence resulting in an imbalance in favor of excitatory NT. The situation is further aggravated by the enhanced activity of excitatory NT glutamate, the receptors for which remain elevated even after withdrawl of alcohol. Both these effects have the cumulative effect of hyperexcitability, which leads to craving for alcohol and withdrawl symptoms.
Added to this is the hetrologous adaptation of brain, i.e the homeostatic response in one system as result of changes in another system. It is very difficult to discern these changes more so because they are not mutually exclusive. And therefore doubts arise as to which one of these neurochemical pathway is actually responsible for
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