2-Minute Neuroscience: GABA

In this video I discuss the neurotransmitter gamma-aminobutyric acid, or GABA. GABA is the primary inhibitory neurotransmitter in the human nervous system; its effects generally involve making neurons less likely to fire action potentials or release neurotransmitters. GABA acts at both ionotropic (GABAa) and metabotropic (GABAb) receptors, and its action is terminated by a transporter called the GABA transporter. Several drugs like alcohol and benzodiazepines cause increased GABA activity, which is associated with sedative effects.

TRANSCRIPT:

Welcome to 2 minute neuroscience, where I simplistically 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.

REFERENCE:

Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, McNamara JO, White LE. Neuroscience. 4th ed. Sunderland, MA. Sinauer Associates; 2008.