Plasticity mechanisms underlying mGluR-induced epileptogenesis.

Transient application of group I metabotropic glutamate receptor (mGluR) agonists to hippocampal slices produces ictal-like discharges that persist for hours after the removal of the agonist. This effect of group I mGluR stimulation--converting a 'normal' hippocampal slice into an 'epileptic-like' one--may represent a form of epileptogenesis. Because this epileptogenic process can be induced in vitro and it occurs within hours, it has been possible to examine the cellular and transduction processes underlying the generation and long-term maintenance of ictal-like bursts. ImGluR(V), a voltage-dependent depolarizing current activated by group I mGluR agonists, appears to play an important role in the expression of the ictal-like bursts. Long-term activation of ImGluR(V) following mGluR stimulation is a possible plastic change that enables the long-term maintenance of ictal discharges. Induction of ImGluR(V) may represent a cellular event underlying the mGluR-induced epileptogenesis.