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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 benzodiazepines.
Benzodiazepines are a class of drugs named for their chemical structure that are commonly
used to treat anxiety disorders and sleep-related disorders.
They include well-known drugs like valium, xanax, and klonopin.
There are dozens of drugs in the benzodiazepine class, but the mechanism by which they all
exert their effects is thought to be similar.
The sedating and anxiety-reducing effects of benzodiazepines are believed to be attributable
to the drugs’ actions at receptors for the neurotransmitter gamma-aminobutyic acid, or
GABA.
In particular, benzodiazepines act at a subtype of GABA receptors called the GABAa receptor;
GABAa receptors that also bind benzodiazepines are sometimes called benzodiazepine receptors.
When benzodiazepines bind, or attach, to the GABA receptor, they bind at a location separate
from where GABA itself binds, and exert an influence over GABA binding.
This type of action is called an allosteric effect, and in the case of benzodiazepines
it results in increased action at the GABA receptor.
There is not complete consensus on exactly how benzodiazepine binding affects activity
at the GABA receptor but there is evidence to suggest that it increases the likelihood
that GABA binding will activate the receptor and/or increases the effect that GABA has
when it binds to the receptor.
That effect is to open an ion channel and allow the passage of negatively charged chloride
ions into the neuron.
This influx of negatively charged ions pushes the membrane potential further from zero,
or hyperpolarizes it, and makes it less likely the neuron will fire an action potential.
This type of neural inhibition is the basis for the effects of benzodiazepines, for by
inhibiting the activity of neurons that make up networks involved with anxiety and arousal,
the drugs are able to produce calming effects.