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Journal of Neuroscience, Vol 12, 3042-3053, Copyright © 1992 by Society for Neuroscience
Desensitization of GABA-activated currents and channels in cultured cortical neurons
MP Frosch, SA Lipton and MA Dichter
Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Application of GABA to rat neocortical neurons maintained in cell culture
produced a response that declined over several seconds, even in the
continued presence of agonist. The decrement could be attributed to both a
redistribution of Cl- and a true decline in GABA-induced membrane
conductance, or desensitization. The extent and rate of desensitization
were dose dependent in a manner similar to the dose dependence of the
GABA-induced current, but were not related to the absolute magnitude of the
current or to the charge transfer. Bicuculline slowed desensitization while
diazepam enhanced the rate of desensitization, consistent with a
localization of desensitization to the agonist-receptor binding site. When
measured in the whole-cell recording mode, desensitization was voltage
dependent, becoming much slower as the membrane was depolarized. Changes in
extracellular or intracellular [Ca2+] did not appear to grossly affect the
desensitization process or its voltage dependence. GABA-activated single
channels, recorded in the outside-out configuration, also desensitized in
the continued presence of agonist. However, desensitization differed from
that seen in the same neurons in the whole-cell mode. Desensitization was
considerably more rapid and did not show any voltage sensitivity. Moreover,
single-channel responses often failed to recover after only a few exposures
to agonist. Desensitization of GABA responses may play a role in the
regulation of cortical inhibition, especially under conditions of intense
excitatory and inhibitory synaptic activation.
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