etoh abuse pathophysiology
Several neuron-behavioural effects of alcohol abuse (etoh abuse) have been related to the development of alcohol dependence. The pleasurable and stimulant effects of alcohol are mediated by a dopamine pathway projecting from the ventral segmental area to the nucleus encumbers.  Repeated, excessive alcohol ingestion sensitizes this pathway and leads to the development of dependence. Long-term exposure to alcohol causes adaptive changes in several neurotransmitter systems, including down-regulation of inhibitory neuronal gamma-aminobutyric acid receptors, up-regulation of excitation glutamate receptors, and increased central nor-epinephrine (noradrenaline) activity.
Discontinuation of alcohol ingestion leaves this excitatory state unopposed, resulting in the nervous system hyperactivity and dysfunction that characterize alcohol withdrawal. It has also been suggested that withdrawal symptoms intensify as withdrawal episodes grow in number, a phenomenon called 'kindling'.
Continuing to clarify the specific neurotransmitters associated with both the behavioral effects of alcohol and the development of alcohol dependence may yield potential targets for drug therapy to treat dependence.