RSA 2005 Abstracts
DUKE UNIVERSITY MEDICAL CENTER, DURHAM
ETHANOL EFFECTS ON POLYSYNAPTIC PATHWAYS FROM
BASOLATERAL AMYGDALA TO CENTRAL AMYGDALA
Maeng-Hee Kang-Parka and Scott D Moore
Department of Psychiatry, Duke University Medical Center, Durham, NC
27710, USA. Research Service, Veterans AdministrationMedical Center, 508
Fulton street, Neurology Research Building 16, Room 25, Durham, NC 27705,
USA
Effects of ethanol on GABAergic and glutamatergic neurotransmission are
well characterized in central amygdala (Roberto et al. J Neurosci 24:
1594-603, 2004; Roberto et al. PNAS 100:2053-8, 2003), and these effects
are implicated in the anxiolytic and rewarding actions of ethanol. We
further examined the effects of ethanol on presumed polysynaptic pathways
from basolateral amygdala to central amygdala using whole cell patch recordings
in a rat brain slice preparation. Central amygdala neurons were patched
using a cesium-based internal solutions and synaptic responses were evoked
by stimulation within the basolateral amygdala. GABAergic inhibitory currents
were isolated by holding neurons at 0 mV, near the reversal potential
for glutamatergic excitatory neurotransmission. Application of either
the glutamate receptor antagonist DNQX or the GABAA receptor antagonist
bicuculline abolished this GABAergic inhibitory currents, indicating that
this response is mediated through glutamatergic activation of GABAergic
neurons. Bath application of ethanol (40 mM) enhanced the polysynaptically-activated
GABAergic responses (n=7). However, this effect was smaller than ethanol
effects on monosynaptically-activated GABAergic responses in central amygdala.
We speculate that this finding is due to ethanols reduction of the
excitatory glutamatergic input from basolateral amygdala. In addition,
we have begun testing the effects of neuromodulators such as endocannabinoids
and opioid peptides that may also be involved in actions of ethanol on
polysynaptically-activated GABAA receptor-mediated synaptic responses.
Further studies of this system may elucidate effects of ethanol in a brain
network critical to its anxiolytic and rewarding actions.
This study was supported by grants from the National Institute of Alcohol
Abuse and Alcoholism, NIH (UO1 AA013498 -INIA Project) and VA Merit Review.
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