In the inhibitory neurons of the amygdala, the arrival of an action potential at the axon terminal causes the release of GABA into the synaptic cleft. Recognition by GABAa post-synaptic receptors causes an influx of chloride through the post-synaptic cell membrane, decreasing the effectiveness of EPSPs and thus decreasing the ability of that neuron to fire action potentials. If no action potential is fired in this cell, one excitatory circuit in the amygdala has thus been quieted. When this inhibitory action occurs in many circuits at the same time, the activity of the amygdala as a whole decreases, and it fires less excitatory signals to other areas of the brain. This in turn leads to a reduction in the physiological and psychological markers of stress and anxiety. To learn more about anxiety disorders, go to http://www.nlm.nih.gov/medlineplus/anxiety.html.