Gamma-Aminobutyric acid (GABA) is the second most common neurotransmitter chemical in the human brain. GABA is an inhibitory neurotransmitter--it calms and reduces the activity of neurons. Some anti-anxiety medications work by promoting greater availability of GABA to brain cells.
While many of the basic functions of GABA have become better understood in the last decade, scientists continue to make new discoveries about GABA and the multiple types of GABA receptors, each of which can play a different role in neural cells.
What are Neurotransmitters?
Neurotransmitters are chemical molecules that brain cells (neurons) and nerve cells use to communicate with each other.
These molecules are released from one neuron (the presynaptic neuron) and travel across a gap (known as a synapse) to attach themselves to a specific receptor site on an opposing neuron (the postsynaptic neuron). When molecules of a given neurotransmitter dock at its dedicated receptor site, specific functions are activated in the receiving cell.
The neurotransmitter may then be re-released back into the synapse for re-uptake into the presynaptic neuron, at which point the transmission process can be repeated.
What Does GABA Do?
GABA is known as an inhibitory neurotransmitter. This means that when it docks at the receptor site of a neuron, it reduces the activity level of that neuron and makes it less likely to fire an electrical signal ("action potential").
GABA achieves this because GABA receptor sites also control the admission of chloride ions into neurons and potassium ions out of neurons. Chloride increases the negative electrical charge within the neuron, and potassium increases the positive charge outside the neuron. This makes it more difficult for the neuron to fire the action potential and excite adjoining neurons.
How Does GABA Affect Psychology and Physiology?
Because GABA is an inhibitory neurotransmitter, it is involved in processes in which neural activity is reduced, such as anxiety reduction, calming, and release of tension.
Some anti-anxiety medications like benzodiazepines and barbiturates primarily work by increasing the amount of GABA in the synapses that is available to bond to GABA receptor sites. Alcohol also promotes the influx of chloride ions into brain cells, and so amplifies the normal effects of GABA.
Caffeine, on the other hand, reduces the available GABA in the synapse, promoting effects like nervousness, anxiety, and difficulty sleeping.
The calming and inhibitory effects of GABA upon neuronal activity also has important physiological effects. For example, the cardiac vagal neurons (CVNs) are areas of the brain that moderate and slow heart rate, keeping it from becoming too rapid. GABA's inhibitory effect upon these neurons can cause heart rate to increase.
Medications that act upon GABA receptors are known as "GABAergic" drugs.