The Dependence of AlcoholicsBbrain on Alcohol - Essay Example

The explanation of the dependence of alcoholics’ brains on alcohol lies in neuronal communication mechanisms. The communication between two nerve cells is through electric signals inside the cells and chemical signals or neurotransmitters between the cells. The gap between two nerve cells, termed as synapse (fig.1) is traversed by small molecules known as neurotransmitters (NT) released by the signal emitting neuron and received by the receptors on the signal receiving neuron. This is followed by a series of events which are the results of the nature of specific NT (i.e. 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 rewarding process: Dopamine and serotonin.

In initial exposure, alcohol induces the production of dopamine, which onsets the encoding of these incidences as environment-linked memories in the cortex of the 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 suppressing the neuronal activity of receptor cells. Here one of the key features of the 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 withdrawal 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 withdrawal of alcohol.