Co-existence of GABA and Glu in the hippocampal granule cells: implications for epilepsy

The granule cells of the Dentate Gyrus are one of the most exciting and intriguing cells in the central nervous system. Besides containing and releasing Glu, they have been shown to contain and release peptides (somatostatin, neuropeptide Y, neurokinin B, cholecystokinin, dynorphin, enkephalin), Zn(++) ion, and brain-derived neurotrophic factor (BDNF). The recent addition of GABA to this list suggests that these cells can also function as inhibitory cells. Indeed, evidence has been presented of co-localization of all markers of the GABAergic phenotype in granule cells: GABA, the enzyme for its synthesis (Glu decarboxylase) and the membrane and vesicular transporters of GABA. These markers of the GABAergic phenotype are up-regulated after epileptic seizures. When this occurs, monosynaptic GABA receptor-mediated transmission emerges in the mossy fiber synapse thus restraining excitation and mediating antiepileptic and neuroprotective actions.