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In primary cultures of cerebellar granule cells kainate produced marked influx of 45Ca2+, partially sensitive to the N-methyl-D-aspartate (NMDA) antagonist, 3-(?)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), indicating involvement of an NMDA receptor-sensitive component that may be secondary to kinate-induced glutamate release.Sodium removal partially inhibited kainate's effect.Quisqualate also produced influx of 45Ca2+, but with lower efficiacy and higher potency than kainate.This action of quiqualate was uneffected by CPP and by sodium removal.Preincubation of cells with the plant lectin concavalin A(Con A), but not with irs succinyl derivative, enhanced quisqualate -induced calcium influx, and to a lesser extend kainate' effect.Inclusion of quisqualate in preincubation medium antagonized Con A potention of quisqualate response.Also Con A was ineffective when included in the incubation medium only, without preincubation.Preincubation of rat brain cortical membranes with Con A but not with succinyl Con A increased the binding of the AMPA receptor agonist. The results suggest that Con A enhancement of quisqualate response possibly involves the modification of an AMPA recogintion site requires preincubation in the absence of an agonist (here quisqualate).
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