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Vol. 283, Issue 2, 969-976, November 1997
-Aminobutyric
AcidA Receptor Blockade in the Basolateral Amygdala of
Rats1
Department of Psychiatry, Pharmacology and Toxicology, and Program
in Medical Neurobiology, Indiana University School of Medicine,
Indianapolis, Indiana
Blockade of
-aminobutyric acid (GABAA)
receptors in the anterior basolateral amygdala (BLA) with bicuculline
methiodide results in an increase in heart rate, blood pressure and
"anxiety" in rats. Glutamate receptors in the BLA are also reported
to be involved in eliciting anxiety responses. The purpose of this
study was to investigate the interaction between GABAergic inhibition
and glutamatergic excitation in the BLA. Male Wistar rats were
implanted with femoral arterial catheters and bilateral chronic
microinjection cannulae into the BLA. Each animal was injected with
either artificial cerebrospinal fluid (100 nl), bicuculline methiodide
(20 pmol/100 nl) or bicuculline methiodide + one dose of an antagonist
of either the N-methyl-D-aspartate receptor [AP5 (20 and
100 pmol) and dizocilpine (25 and 125 pmol)] or the
non-N-methyl-D-aspartate ionotropic receptor [CNQX (10 and
50 pmol) and GYKI 52466 (50 and 250 pmol)]. Increases in heart rate,
blood pressure and "anxiety" (as measured in the social interaction
test) observed in rats after bicuculline methiodide injections into the
BLA were blocked in a dose dependent manner with the concurrent
injections of either N-methyl-D-aspartate or
non-N-methyl-D-aspartate antagonists, suggesting that
activation of both subtypes of glutamate ionotropic receptors may be
necessary for the responses elicited by GABAA receptor
blockade in the anterior basolateral amygdala.
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