Kainate injury to cultured basal forebrain cholinergic neurons is Ca2+ dependent

Abstract

WHILE exposure times of several hours or more are needed for kainate to induce widespread degeneration of most cortical or basal forebrain neurons, basal forebrain cholinergic neurons, as identified by choline acetyltransferase immunocytochemistry, were substantially damaged by brief (45 min) kainate exposures. This rapidly triggered damage to basal forebrain cholinergic neurons is Ca2+ dependent. Also, basal forebrain cholinergic neurons have unusually large elevations in intracellular Ca2+ concentration in response to kainate, and generally exhibit kainate-activated Co2+ uptake, suggesting that they possess Ca(2+)-permeable AMPA/kainate receptor-gated channels. The heightened vulnerability of basal forebrain cholinergic neurons to kainate toxicity may reflect rapid Ca2+ entry through Ca(2+)-permeable AMPA/kainate channels.