GABA(B) receptor-mediated presynaptic inhibition of glycinergic transmission onto substantia gelatinosa neurons in the rat spinal cord

In-Sun Choi, Jin-Hwa Cho, Seok-Gwon Jeong, Jung-Soo Hong, Sang-Jung Kim, Jun Kim, Maan-Gee Lee, Byung-Ju Choi, Il-Sung Jang
Pain 2008 August 31, 138 (2): 330-42
The GABA(B) receptor-mediated presynaptic inhibition of glycinergic transmission was studied from 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 acid and 10 microM SR95531. In these conditions, baclofen (30 microM), a selective GABA(B) receptor agonist, greatly reduced the amplitude of glycinergic IPSCs and increased the paired-pulse ratio. Such effects were completely blocked by 3 microM 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 microM 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 microM concentration completely blocked glycinergic synaptic depression, but at a 3 microM 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.

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