Glutamatergic transmission of neuronal responses to carbachol in rat dorsal cochlear nucleus slices

This study found that glutamate receptor antagonists block the excitatory e ffects of carbachol, a cholinergic agonist, on bursting neurons in the dors al cochlear nucleus of rat brain slices. Among antagonists for glutamate re ceptor subtypes, those for non-N-methyl-D-aspartate ionotropic glutamate re ceptors were more potent than those for N-methyl-D-aspartate receptors. The glutamate receptor antagonists did not block the effects of carbachol on r egularly firing neurons in the dorsal cochlear nucleus of the same slices. Antagonists for GABA or glycine receptors did not alter the effects of carb achol on bursting neurons. Effects of carbachol on bursting activity could be mimicked by application of glutamate or its agonist, alpha-amino-3-hydro xy-5-methylisoxazole-4-propionate, whose effects were not blocked by synapt ic blockade. During carbachol application, increased release of glutamate a nd glycine from the dorsal cochlear nucleus part of brain slices was measur ed using high-performance liquid chromatography. Release of other amino aci ds showed no significant change. The results suggest that, in rat dorsal cochlear nucleus, cholinergic effec ts on regular and bursting spontaneous firing occur through different mecha nisms. Cholinergic effects on regular neurons (which include fusiform cells ) are direct, through muscarinic receptors. Cholinergic effects on bursting neurons (which include cartwheel cells) are indirect and involve glutamate rgic neurotransmission, mostly via non-N-methyl-D-aspartate ionotropic rece ptors. The granule cell-parallel fiber pathway may be involved in this glut amatergic transmission. (C) 1999 IBRO. Published by Elsevier Science Ltd.