| Literature DB >> 6295548 |
J C Hackman, D Auslander, V Grayson, R A Davidoff.
Abstract
GABA (gamma-aminobutyric acid) depolarizes the terminals of primary afferent fibers of the in vitro hemisected frog spinal cord. During sustained or repetitive exposure to GABA or to muscimol, the amplitude of the depolarization is characterized by a rapid and exponential decline to a steady plateau level (desensitization). Desensitization to muscimol was eliminated by removal of Ca2+ and addition of Mn2+ to the superfusate--a finding consistent with the presence of 'receptor' ('true') desensitization (i.e., receptor inactivation). GABA desensitization was significantly reduced by exposure of the cord to either low Na+, low temperature, ouabain, dinitrophenol, (+/-)-nipecotic acid, or cis-1,3-aminocyclohexanecarboxylic acid. These treatments also significantly decreased the high affinity uptake of GABA when the latter process was studied by incubating frog spinal slices in Ringer's solution containing a low concentration of [3H]GABA. These results suggest that cellular transport processes can influence the form of GABA responses and indicate that neuronal removal of GABA is responsible in part for GABA desensitization.Entities:
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Year: 1982 PMID: 6295548 DOI: 10.1016/0006-8993(82)90681-3
Source DB: PubMed Journal: Brain Res ISSN: 0006-8993 Impact factor: 3.252