KAINATE INJURY TO CULTURED BASAL FOREBRAIN CHOLINERGIC NEURONS IS CA2+ DEPENDENT

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