Release of [ 3h]- l-glutamate by stimulation of nicotinic acetylcholine receptors in rat cerebellar slices

Abstract

This is a neurochemical study which shows that nicotine acting through α7-containing nicotinic acetylcholine receptors promotes the release of [ 3H]-glutamate from rat cerebellar slices. Release evoked by half maximal concentration of nicotine (100 μM) was blocked by α-bungarotoxin and in a calcium-free medium, suggesting an effect mediated by an α7 receptor. Dihydro-β-erythroidine and mecamylamine were effective only at very high concentrations, excluding the participation of heteromeric receptors. The effect of nicotine was partially blocked by inhibitors of glutamatergic receptors dl-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3-dione, indicating a glutamate-induced glutamate release. Nicotine-evoked response was dependent on activation of tetrodotoxin sensitive sodium channels. Therefore, here we show that glutamate released by stimulation of α7-containing nicotinic receptors, located preterminal and/or postsynaptically, evokes a further glutamate release in adult rat cerebellar slices.