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Electrophysiological studies show that the decrease in the amount of gamma-aminobutyric acid (GABA) present in the temporal lobe of humans is because of a decrease in the number of GABA transporters which affects the release of GABA. In the epileptogenic hippocampi, the potassium-stimulated release of GABA increases while the glutamate-induced, calcium-independent release of GABA decreases. However, the number of GABA containing cells and receptors in the neurons of the epileptogenic hippocampi is the same as that in normal neurons. GABA is probably necessary to mediate synaptic transmission and decreases are linked to epileptic seizures.

The 5-hydroxytryptamine-2c (5-HT2c) receptor is vital for the serotonergic control of feeding appetite. Mice with insufficient 5-HT2c receptors are overweight due to a behavioral disorder not a metabolic abnormality. A loss in the 5-HT2c function also results in a diminished seizure threshold and a vigorous advancement of seizure activity. The 5-HT2c receptors link to serotonin, a monoaminergic neurotransmitter involved in the mediation of the tonic inhibition of neuronal network excitability.

Studies conducted on the role of the neurotransmitter gamma-amino butyric acid (GABA) show that the amount of GABA in the hippocampus affected by epilepsy is less than in the normal hippocampus. The number of neurons which contain GABA and GABA receptors are unaffected in the affected temporal lobe but the number of GABA transporters are less. In the epileptic hippocampus, the release of GABA is mainly vesicular and the non-vesicular release decreases compared to a normal hippocampus. Inhibition of GABA activity causes epileptic seizures.