Neuropeptide Y and Epilepsy

Abstract

It is a central tenet of the epilepsy field that seizures result from the imbalance of excitation over inhibition (1). The bulk of excitation is mediated by the neurotransmitter glutamate, whereas inhibition results mainly from the actions of gamma-aminobutyric acid (GABA). In the neocortex and hippocampus, the intrinsic sources of GABA are the interneurons, which lately have come under intense scrutiny. It has become clear that a large number of distinct types of interneurons can be differentiated in part by the array of neuropeptides they coexpress (cf. (2)). Evidence is emerging that the neuropeptide complement of interneurons plays important roles in the way that interneurons regulate excitability. Here we discuss what is known about the relation of one well-characterized neuropeptide, neuropeptide Y (NPY), and epilepsy in experimental animals and humans, and suggest possible roles for the receptors as targets for the control of excessive excitation in epilepsy.