Nicotinic receptors regulate the release of glycine onto lamina X neurones of the rat spinal cord.

Whole-cell patch clamp recordings were performed on neurones in the lamina X of rat spinal cord slices in order to characterize glycinergic synaptic currents and their modulation by nicotinic acetylcholine receptors. In the presence of TTX, bicuculline and kynurenic acid, glycine-induced currents and miniature glycinergic postsynaptic currents (mIPSCs) were recorded. These currents reversed near the chloride ion equilibrium potential and were blocked by strychnine (1 microM). A selective nicotinic acetylcholine receptor (nAChR) agonist 1,1-dimethyl-4-phenyl-piperazinium (DMPP), increased the frequency of glycinergic mIPSCs without altering significantly their amplitude distributions or their kinetic properties. The effects of DMPP were mimicked by different nAChRs agonists with the following apparent order of potency: ACh > DMPP > nicotine > cytisine. The effect of DMPP on mIPSCs was blocked by both d-tubocurarine and hexamethonium, and was reduced by dihydro-beta-erythroidine and methyllycaconitine (MLA), antagonists of non alpha7- and alpha7-containing nAChRs, respectively. In the absence of TTX, strychnine-sensitive glycinergic electrically evoked postsynaptic currents (eIPSCs) could be recorded. DMPP blocked the appearance of electrically evoked IPSCs while still inducing the appearance of spontaneous glycine IPSCs. These data demonstrate that neurones surrounding the central canal of the spinal cord present a glycinergic synaptic transmission which is modulated by terminal nAChRs.