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

Cited 15 time in Web of Science Cited 16 time in Scopus
Authors
Choi, In-Sun; Cho, Jin-Hwa; Jeong, Seok-Gwon; Hong, Jung-Soo; Kim, Sang-Jung; Kim, Jun; Lee, Maan-Gee; Choi, Byung-Ju; Jang, Il-Sung
Issue Date
2008-02-09
Publisher
Elsevier
Citation
Pain. 2008 Aug 138(2):330-342
Keywords
AnimalsBaclofen/pharmacologyGlycine/antagonists & inhibitors/*physiologyInhibitory Postsynaptic Potentials/drug effects/physiologyNeural Inhibition/drug effects/*physiologyNeurons/drug effects/physiologyRatsRats, Sprague-DawleyReceptors, GABA-B/agonists/*physiologyReceptors, Presynaptic/agonists/antagonists & inhibitors/*physiologySpinal Cord/drug effects/physiologySubstantia Gelatinosa/drug effects/*physiologySynaptic Transmission/drug effects/*physiology
Abstract
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.
ISSN
1872-6623 (Electronic)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18258370

http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T0K-4RS9STC-5-W&_cdi=4865&_user=168665&_orig=search&_coverDate=08%2F31%2F2008&_sk=998619997&view=c&wchp=dGLbVtb-zSkzS&md5=1417ae4308c4809872c1bc4612164296&ie=/sdarticle.pdf

http://hdl.handle.net/10371/68121
DOI
https://doi.org/10.1016/j.pain.2008.01.005
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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