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Journal of Neuroscience, Vol 14, 1079-1090, Copyright © 1994 by Society for Neuroscience
Presynaptic inhibition by GABA is mediated via two distinct GABA receptors with novel pharmacology
G Matthews, GS Ayoub and R Heidelberger
Department of Neurobiology and Behavior, State University of New York, Stony Brook 11794-5230.
Mechanisms of presynaptic inhibition were examined in giant presynaptic
terminals of retinal bipolar neurons, which receive GABAergic feedback
synapses from amacrine cells. Two distinct inhibitory actions of GABA are
present in the terminals: a GABAA-like Cl conductance and a GABAB- like
inhibition of voltage-dependent Ca current. Both of the receptors
underlying these actions have unusual pharmacology that fits neither GABAA
nor GABAB classifications. The GABA-activated Cl conductance was not
blocked by the classical GABAA antagonist bicuculline, while the inhibition
of Ca current was neither mimicked by the GABAB agonist baclofen nor
blocked by the GABAB antagonist 2-hydroxysaclofen. The "GABAC" agonist
cis-4-aminocrotonic acid (CACA) both activated the Cl conductance and
inhibited Ca current, but the inhibition of Ca current was observed at much
lower concentrations of CACA (< 1 microM) than was the activation of the
Cl conductance (K1/2 = 50 microM). Thus, by the criterion of being
insensitive to both bicuculline and baclofen, both GABA receptors qualify
as potential GABAC receptors. However, it is argued on functional grounds
that the two GABA receptors coupled to Cl channels and to Ca channels are
best regarded as members of the GABAA and GABAB families, respectively.
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