Activation of dopaminergic neurons modulates ventral pallidal responses evoked by Amygdala stimulation

doi:10.1016/0306-4522(94)90347-6

Neuroscience

Volume 62, Issue 4, October 1994, Pages 1103-1119

https://doi.org/10.1016/0306-4522(94)90347-6 Get rights and content

Abstract

The ventral pallidum is a basal forebrain region that is thought to integrate cognitive processes with motoric behaviors. These functions are influenced by ventral pallidal inputs, which include projections from the amygdala and the ventral tegmental area/substantia nigra zona compacta. By examining the consequences of this convergence at the neuronal level, the present study indicates that electrical activation of ventral tegmental regions releases dopamine in the ventral pallidum which subsequently modulates pallidal electrophysiological responses evoked by stimulating the amygdala.

Stimulation-evoked responses were characterized for extracellular single unit recordings of spontaneously active ventral pallidal neurons from chloral hydrate anesthetized rats. Stimulation of the amygdala evoked short latency (⩽ 12 ms; possibly monosynaptic) and/or long latency (> 12 ms; polysynaptic) responses in all ventral pallidal neurons tested. Fifty-nine per cent of the tested neurons responded to ventral tegmental stimulation with short latency inhibition, and these neurons were often sensitive to microiontophoretically applied dopamine. Iontophoresis of dopamine antagonists SCH23390 (a Dl antagonist) or sulpiride (a D2 antagonist) attenuated the ventral tegmental-induced inhibitions. These observations indicate that the evoked responding was the result of endogenously released dopamine, and that D1 and D2 receptors were involved in this effect.

Ninety-two per cent of the ventral pallidal neurons that demonstrated short latency responses to amygdala stimulation also exhibited short latency responses to activation of the ventral tegmentum. This suggests that these inputs often converge onto the same pallidal neurons. Amygdala-evoked responses were consistently attenuated by prior stimulation of the ventral tegmentum. Similarly, microiontophoretic ejection of dopamine attenuated amygdala-evoked effects. These results indicate that dopamine modulates amygdala-evoked pallidal responses. Such modulation may contribute to the integrative functions of the ventral pallidum.

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Activation of dopaminergic neurons modulates ventral pallidal responses evoked by Amygdala stimulation

Abstract

Brain Res.

Brain Res.

Eur. J. Pharmac.

Neurosci. Lett.

Neuroscience

Neuroscience

Trends Neurosci.

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Neuroscience

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Neuroscience

Neuroscience

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Eur. J. Pharmac.

Life Sci.

Neuroscience

Neuropharmacology

Neurosci. Lett.

Eur. J. Pharmac.

Neurosci. Lett.

Brain Res.

Brain Res.

Brain Res.

Comp. Biochem, Physiol.

Neuroscience

Brain Res.

Neurosci. Lett.

Neuroscience

Distribution of D1 and D2 dopamine receptors in the basai ganglia of the cat determined by quantitative autoradiography

J. comp. Neurol.

Pre- and postsynaptic striatal dopamine receptors: differential sensitivity to apomorphine inhibition of [3H]dopamine and [14C]GABA release in vitro

J. Pharm. Pharmac.

Central cholinergic systems: synopsis of anatomy and overview of physiology and pathology

Organization of the basolateral amygdala

Acta Neurol. Scand.

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J. comp. Neurol.

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J. Neural Transm.

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A. Rev. Pharmac. Toxicol.

Action of apomorphine, bromocriptine and lergotrile on γ-aminobutyric acid and acetylcholine release in nucleus accumbens and corpus striatum

J. Neural Transm.

Microiontophoresis and the central nervous system

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Biol. Rev.

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J. camp. Neurol.

Substantia nigra 6-hydroxydopamine lesions alter dopaminergic synaptic markers in the nucleus basalis magnocellularis and striatum of rats

Synapse

Distribution of D₁ and D₂ dopamine receptors in the basai ganglia of the cat determined by quantitative autoradiography

Pre- and postsynaptic striatal dopamine receptors: differential sensitivity to apomorphine inhibition of [³H]dopamine and [₁₄C]GABA release in vitro