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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
- Issue Date
- 2008-02-09
- Publisher
- Elsevier
- Citation
- Pain. 2008 Aug 138(2):330-342
- Keywords
- Animals ; Baclofen/pharmacology ; Glycine/antagonists & inhibitors/*physiology ; Inhibitory Postsynaptic Potentials/drug effects/physiology ; Neural Inhibition/drug effects/*physiology ; Neurons/drug effects/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-B/agonists/*physiology ; Receptors, Presynaptic/agonists/antagonists & inhibitors/*physiology ; Spinal Cord/drug effects/physiology ; Substantia Gelatinosa/drug effects/*physiology ; Synaptic 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
https://hdl.handle.net/10371/68121
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