Neurobiological Effects of Drinking

Alcohol is a socially acceptable psychoactive drug in spite of its potentially negative short- and long-term effects on health. The neurobiological mechanisms of ethanol's psychoactive and addictive properties are well-understood, but complicated. Many of its effects are dose-dependent, with different effects along the dosage timeline. Many scientists argue the addictive qualities of ethanol come from the interaction between inherent genetic abnormality and neurobiological changes caused by chronic ethanol consumption.

Gamma Amino Butyric Acid

• Alcohol generates the majority of its effects in the brain from its effects on GABA-A receptors. These receptors are the dominant postsynaptic receptors for GABA, an inhibitory neurotransmitter. Alcohol consumption creates a central nervous system depressant effect via this mechanism. When exposed to high doses of alcohol over a long period of time, the structure of cellular receptor proteins change, increasing the tolerance to alcohol, but creating hyper-excitability, anxiety, and tremors when alcohol is not present. Glutamate receptors also may develop increased sensitivity in response to chronic alcohol exposure.

Dopamine

• Much of alcohol's behavioral reinforcing characteristics are thought to be caused by its effects on the mesocorticolimbic dopamine system. This system is made up of dopamine-releasing neurons that connect the medial prefrontal cortex and nucleus accumbens with the ventral tegmentum, effectively tying the reward centers of the reptilian brain with the behavioral centers of the midbrain. This is substantiated by studies on the brains of alcoholics, many of which show abnormal and low-functioning neurotransmitter systems, especially in the mesocorticolimbic dopamine system. Alcohol consumption may compensate for these deficiencies in alcoholics. Through its effects on the receptors of neurotransmitters affecting the dopaminergic system, alcohol causes an increase in limbic system dopamine levels.

Endorphins

• Ethanol also affects the binding attributes and synthesis of opioid peptide receptors. In fact, it is thought that it may stimulate the release of beta-endorphins, endogenous opioid neurotransmitters that create the feelings of euphoria and anesthesia that sometimes are a part of alcohol's psychoactive experience. The experimental administration of the opioid antagonist drug naltrexone appears to reduce the craving for alcohol, lending credence to this theory and to its use in the treatment of alcoholism.

Serotonin

• Abnormalities in the serotonin levels of alcoholics also have been observed, although it is unclear whether low serotonin levels promote alcohol seeking behavior or whether chronic alcohol use lowers serotonin levels. Human and animal studies exist supporting both theories, leading some to posit a combined effect. It is known that drugs which promote the release or prevent the re-uptake of synaptic serotonin result in a decrease of voluntary self-administration of alcohol in rats.