GABAB receptor-mediated presynaptic inhibition of glycinergic transmission onto substantia gelatinosa neurons in the rat spinal cord

The GABA(B) receptor-mediated presynaptic inhibition of glycinergic transmission was studied froth young rat substantia gelatinosa (SG) neurons using a conventional whole-cell patch clamp technique. Action potential-dependent glycinergic inhibitory postsynaptic currents (IPSCs) were recorded from SG neurons in the presence of 3 mM kynurenic geld and 10 mu M SR95531. In these conditions, baclofen (30 mu M), a selective GABA(B) receptor agonist, greatly reduced the amplitude of glycinergic IPSCs and increased the paired-pulse ratio. Such elects were completely blocked by 3 mu M CGP55845, a selective GABA(B) receptor antagonist. indicating that the activation of presynaptic GABA(B) receptors decreases glycinergic synaptic transmission. Glycinergic IPSCs were largely dependent on Ca2+ influxes passing through presynaptic N- and P/Q-type Ca2+ channels. and these channels contributed equally to the baclofen-induced inhibition of glycinergic IPSCs. However, the baclofen-induced inhibition of glycinergic IPSCs was not affected by either 100 mu M SQ22536. an adenylyl cyclase inhibitor. or 1 mM Ba2+, a G-protein coupled inwardly rectifying K+ channel blocker. During the train stimulation (10 pulses at 20 Hz). which caused a marked synaptic depression of glycinergic IPSCs, baclofen at a 30 mu M concentration completely blocked glycinergic synaptic depression. but at a 3 IN concentration it largely preserved glycinergic synaptic depression. Such GABA(B) receptor-mediated dynamic changes in short-term synaptic plasticity of glycinergic transmission onto SG neurons might contribute to the central processing of sensory signals. (C) 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.