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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 gamma-aminobutyric acid, or GABA.
Although GABA’s primary functions are as a neurotransmitter, it has the structure of
an amino acid and thus is referred to as an amino acid neurotransmitter.
It is synthesized from another amino acid neurotransmitter, glutamate, in a reaction
catalyzed by the enzyme glutamic acid decarboxylase.
The function of GABA changes over the course of neural development, but in the mature brain
it acts primarily as an inhibitory neurotransmitter; in other words when GABA interacts with the
receptors of a neuron, it generally makes the neuron less likely to fire an action potential
or release neurotransmitters.
There are two types of receptors GABA interacts with, GABAa and GABAb receptors.
GABAa receptors are ionotropic receptors.
When GABA binds to the GABAa receptor, it causes the opening of an associated ion channel
that is permeable to the negatively charged ion chloride.
When negative chloride ions flow into the neuron, they hyperpolarize the membrane potential
of the neuron and make it less likely the neuron will fire an action potential.
GABAb receptors are metabotropic (or g-protein coupled) receptors; when activated they frequently
cause the opening of potassium channels.
These channels allow positively charged potassium ions to flow out of the neuron, again making
the neuron hyperpolarized and less likely to fire an action potential.
The actions of GABA are terminated by proteins called GABA transporters, which transport
GABA from the synaptic cleft into neurons or glial cells where it is degraded primarily
by mitochondrial enzymes.
Because GABA can reduce neural transmission, increased GABA activity can have sedative
effects.
Accordingly, a number of drugs that have such effects, like alcohol and benzodiazepines,
increase activity at the GABA receptor.