GABA(B) 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 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.
Choi
In-Sun
IS
Department of Pharmacology, School of Dentistry, Kyungpook National University, 188-1 Samduk 2 ga-dong, Jung-gu, Daegu 700-412, Republic of Korea Department of Physiology, School of Medicine, Seoul National University, Seoul 110-799, Republic of Korea Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-412, Republic of Korea Brain Science & Engineering Institute, Kyungpook National University, Daegu 700-412, Republic of Korea.
Cho
Jin-Hwa
JH
Jeong
Seok-Gwon
SG
Hong
Jung-Soo
JS
Kim
Sang-Jung
SJ
Kim
Jun
J
Lee
Maan-Gee
MG
Choi
Byung-Ju
BJ
Jang
Il-Sung
IS
D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D058786:GABA-B Receptor Agonists; D005998:Glycine / Q000037:antagonists & inhibitors / Q000502:physiology*; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018080:Receptors, GABA-B / Q000502:physiology*; D017661:Receptors, Presynaptic / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology; D013376:Substantia Gelatinosa / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
D058786:GABA-B Receptor Agonists; D018080:Receptors, GABA-B; D017661:Receptors, Presynaptic; D001418:Baclofen; D005998:Glycine