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.