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 Previous Article
Journal of Neuroscience, Vol 6, 2470-2478, Copyright © 1986 by Society for Neuroscience
Dopamine enhances terminal excitability of hippocampal-accumbens neurons via D2 receptor: role of dopamine in presynaptic inhibition
CR Yang and GJ Mogenson
The effects of dopamine on the axonal terminals of hippocampal-nucleus
accumbens (HIPP-ACC) neurons were investigated in urethane-anesthetized
rats using extracellular single-unit recording techniques. Antidromic
responses recorded in the ventral subiculum of the hippocampus were evoked
by stimulation of the medial accumbens. Baseline terminal excitability of
these neurons, established by threshold stimulation of the accumbens, was
markedly enhanced by conditioning stimulation (10 Hz) of the ventral
tegmental area (VTA), the origin of the mesolimbic dopaminergic neurons.
Iontophoretic application of sulpiride, a selective D2 antagonist, onto the
HIPP-ACC terminals attenuated the increased terminal excitability of these
neurons produced by conditioning VTA stimulation, while intraperitoneal
injection of SCH23390, a selective D1 antagonist, failed to attenuate this
effect. Iontophoretic application of dopamine or its selective D2 agonist,
LY171555, onto the terminals of the HIPP-ACC neurons mimicked the prolonged
enhancement of the terminal excitability produced by VTA stimulation,
whereas SKF38393, a D1 agonist, had no effect. The effects of VTA
stimulation, dopamine and LY171555 application were similar after the
accumbens had been pretreated with ibotenic acid, suggesting a direct
action of dopamine on the axonal terminals of HIPP-ACC neurons, and that
changes in terminal excitability were not mediated via interneurons or
feedback pathways from the accumbens to the hippocampus. Since
iontophoretic application of potassium, a depolarizing agent, also enhanced
the terminal excitability of the HIPP- ACC neurons, it appears that
dopamine depolarized, via D2 receptors, the axonal terminals of HIPP-ACC
neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
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