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Journal of Neurophysiology, Vol 69, Issue 1 286-289, Copyright © 1993 by APS
ARTICLES |
P. G. Wagner and M. S. Dekin
School of Biological Sciences, University of Kentucky, Lexington 40506-0225.
1. Labeled premotor respiratory neurons from neonatal rats in culture were used to study the effects of (+/-)baclofen, a selective gamma-aminobutyric acid (GABA)b receptor agonist known to inhibit rhythmic breathing movements in mammals. Bath application of (+/-)baclofen-activated outward currents in cell-attached patches, suggesting that a second messenger system linked the (+/-)baclofen-activated conductance (GBac) to the GABAb receptor. 2.GBac channels exhibited outward rectification and were insensitive to blockade by Ba2+ and Cs+. The single-channel conductance was 100 pS in symmetrical K+ solutions and decreased as [K+]o was reduced. The reversal potential for the GBac channel shifted 45 mV/decade when [K+]o was changed indicating that it was predominantly selective for K+ ions. These properties were similar to those of the S-channel in Aplysia sensory neurons. 3. The properties of GBac channels were distinct from those associated with the GABAb mediated slow inhibitory postsynaptic potential (IPSP), indicating that GABAb receptors can be associated with more than one type of K+ channel. We propose that GBac channels modulate the repetitive firing activity of premotor respiratory neurons and may also participate in presynaptic inhibition.
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