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The Journal of Neuroscience, August 15, 2001, 21(16):6370-6376
Dopamine D1 and NMDA Receptors Mediate Potentiation
of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens
Neurons
Stan B.
Floresco1,
Charles D.
Blaha2,
Charles
R.
Yang3, and
Anthony G.
Phillips1
1 Department of Psychology, University of British
Columbia, Vancouver, British Columbia, Canada V6T 1Z4,
2 Department of Psychology, Macquarie University, Sydney,
New South Wales, Australia 2109, and 3 Eli Lilly Company,
Neuroscience Research, Lilly Corporate Center, Indianapolis, Indiana
46285-0510
Interactions between the basolateral amygdala (BLA) and the nucleus
accumbens (NAc) mediate reward-related processes that are modulated by
mesoaccumbens dopamine (DA) transmission. The present in
vivo electrophysiological study assessed: (1) changes in the
firing probability of submaximal BLA-evoked single neuronal firing
activity in the NAc after tetanic stimulation of the BLA, and (2) the
functional roles of DA and NMDA receptors in these processes. Tetanic
stimulation of the BLA potentiated BLA-evoked firing activity of NAc
neurons for a short duration (~25 min). This short-term potentiation
was associated with an increase in DA oxidation currents that was
monitored with chronoamperometry. Systemic or iontophoretic application
before BLA tetanus of the D1 receptor antagonist SCH23390,
but not the D2 receptor antagonist sulpiride, abolished the
potentiation of BLA-evoked NAc activity, whereas administration of
SCH23390 3 min after tetanus had no effect. However, systemic
administration of the NMDA antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid
(CPP), either before or after BLA tetanus, abolished the
potentiation of BLA-evoked firing of NAc neurons. These data suggest
that higher-frequency activity in BLA efferents can autoregulate their
excitatory influence over neural activity of NAc neurons by
facilitating the release of DA and activating both DA D1
and NMDA receptors. This may represent a cellular mechanism that
facilitates approach behaviors directed toward reward-related stimuli
that are mediated by BLA-NAc circuitries.
Key words:
nucleus accumbens; basolateral amygdala; dopamine; NMDA; extracellular recording; chronoamperometry
Copyright © 2001 Society for Neuroscience 0270-6474/01/21166370-07$05.00/0
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