Alcohol and the Brain
The consumption of alcohol gives rise to a large number of complex changes within our brain and to its metabolic balance, as alcohol induces simultaneous alterations in the activity of several central stimulating and sedative neural pathways.
The changing ratio of activity between these pathways – dependent on the blood-levels of alcohol which correspond to the time and quantity of consumption – is considered to shape the wide range of pleasant (and less desirable) sensations which are experienced during and after social drinking.
Alcohol’s major and better-known influences on the brain alter the activity of its two most common neurotransmitters: Glutamate and GABA.
Glutamate is the most common excitatory neurotransmitter used within the brain, which after binding to its receptor increases the flow of positively charged ions into the neurons (Depolarization), enhancing their sensitivity and exciting the activity of neural systems. Alcohol interferes with the activity of the Glutamate receptors within the brain, creating an overall sedation of neural pathways, sluggish thought and reduced ability to respond to stimuli.
GABA is the most common inhibitory neurotransmitter used within the brain, which after binding to its receptor increases the flow of negatively charged Chloride ions into the neurons (Hyperpolarization), reducing their sensitivity and sedating the activity of neural systems. Alcohol increases the activity of the GABA receptors within the brain, creating an additional effect of sedation.
Despite these direct interactions, alcohol’s more complexed and unique effects within the brain are observed in neural systems that utilize both Glutamatergic (Glutamate-releasing) and GABAergic (GABA-releasing) neurons. One example of this is the Mesolimbic Pathway of the Reward System in which alcohol induces the release of the neurotransmitter Dopamine:
Dopaminergic (Dopamine-releasing) neurons in the Reward System are inhibited by GABAergic neurons, which are formerly activated by Glutamatergic neurons [1]. As a result of the alcohol-induced impaired Glutamatergic activity, GABAergic neurons are less-activated and therefore enable increased release of Dopamine in the Reward System, which have been previously associated with sensations of pleasure and happiness [2].
Alcohol’s primarily sedative effects on the neuronal systems have been shown to promote an elaborate chain of effects, which can result in a contradicting excitation of neural pathways.
By pinpointing and strategically strengthening alcohol’s excitatory effects along these pathways, such as by increasing the release of Dopamine in the Reward System, we are able to modify the sensations achieved by alcohol consumption and to create a more enjoyable, leveled and healthier experience.
[1] Clapp, P. et al. (2008). ” How adaptation of the brain to alcohol leads to dependence: a pharmacological perspective.” Alcohol Res. Health, 31(4), 310-39.
[2] Sharot T. et al. (2009). “Dopamine Enhances Expectation of Pleasure in Humans.” Curr. Biol., 19(24), 2077-80.
