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Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or
less.
In this installment I will discuss alcohol.
How alcohol acts in the central nervous system is still poorly understood.
Two of the best known effects of alcohol, however, are its actions on GABA and glutamate
receptors.
Alcohol increases GABA activity at a subtype of the GABA receptor known as GABAa.
The mechanism by which this occurs is still not clear, but it is thought that alcohol
may act as a positive allosteric modulator, meaning it binds to a site on the receptor
that is separate from where GABA binds, and increases the effect GABA has when it binds
to the receptor itself.
The immediate effect of this action typically is the inhibition of neural firing.
Alcohol also inhibits the activity of glutamate receptors.
Again, the mechanism for this is not fully understood but because glutamate is generally
excitatory, inhibition by alcohol initially leads to the reduction of neural activity.
A long list of other synaptic actions have been linked to alcohol, including (but not
limited to): activation of serotonin receptors, enhancement of glycine receptor function,
inhibition of adenosine reuptake, inhibition of calcium channels, activation of potassium
channels, and modulation of nicotinic acetylcholine receptor function.
It’s not clear, however, how relevant each of these effects are to the human use of alcohol.
There are also some large-scale effects associated with alcohol.
For example, alcohol stimulates dopamine transmission in the mesolimbic dopamine pathway--an action
thought to be associated with the reinforcement of alcohol consumption.
Alcohol affects motor coordination and balance, potentially in part through its influence
on neurons in the cerebellum.
And it inhibits long-term potentiation and other mechanisms of synaptic plasticity in
the hippocampus, which may contribute to its memory-disrupting effects.