The various inputs received by the amygdala often transmit conflicting signals. It is not uncommon for excitatory and inhibitory neurons to synapse on the same neuron. The arrival of an excitatory signal triggers a wave of depolarization along the membrane of a post-synaptic neuron known as an excitatory post-synaptic potential (EPSP). Inhibitory signals have an opposite effect. Such signals cause a wave of hyperpolarization along the membrane of a post-synaptic cell known as an inhibitory post-synaptic potential (IPSP). When they arrive at the same neuron, these opposing signals travel along the post-synaptic membrane until they reach the axon terminal, where they are then integrated. If enough EPSPs arrive at the axon terminal simultaneously, the membrane potential will rise above threshold, and an action potential will fire. The presence of IPSPs, however, will lower the membrane potential. If enough IPSPs have fired, these inhibitory signals will stop the neuron from firing.

In times of stress, excitatory neurons in the amygdala fire rapidly, sending excitatory signals to other areas of the brain. It is this type of firing that leads to a feeling of panic or fear. The inhibitory interneurons in the amygdala modulate these emotions by releasing GABA. The release of GABA, and its subsequent recognition by post-synaptic receptors like the GABAa receptor, inhibits the excitatory signals that result in feelings of anxiety and fear. GABA thus has a calming, tranquilizing effect on our emotions and prevents us from becoming overwhelmed in stressful situations. GABA is important in maintaining a normal level of firing for all kinds of different systems; for information about GABA and epilepsy, a disease characterized by seizures due to uncontrollable firing of certain neurons, go to