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Inhibition of mu opioid-induced motor activity in the ventral pallidum by D1 receptor blockade

J.E. Alesdatter1, P.W. Kalivas

  • 1Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, WA 99164-6520, USA.

Behavioural Pharmacology
|December 1, 1993
PubMed

Insights

Microinjection of DAMGO into the ventral pallidum causes motor stimulation. Dopamine D1 receptor activation is essential for this effect, as shown by antagonist studies.

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • The ventral pallidum (VP) is implicated in motor control.
  • Opioid peptides, like DAMGO, can influence motor activity.

Purpose of the Study:

  • To investigate the role of dopamine (DA) transmission in the motor stimulant effects of DAMGO in the VP.
  • To determine the specific roles of dopamine D1 and D2 receptors in this response.

Main Methods:

  • Microinjection of DAMGO and various dopamine antagonists (fluphenazine, SCH-23390, raclopride) into the ventral pallidum of rats.
  • Assessment of horizontal and vertical motor activity following microinjections.

Main Results:

  • Coadministration of the D1/D2 antagonist fluphenazine partially reduced DAMGO-induced motor activity.
  • The D1-selective antagonist SCH-23390 dose-dependently reduced motor activity, with a minimum effective dose of 0.3 nmol/side.
  • The D2-selective antagonist raclopride had no effect on DAMGO-induced motor activity.
  • A combination of SCH-23390 and raclopride did not alter the effects of SCH-23390 alone.

Conclusions:

  • Dopamine D1 receptor stimulation is permissive for the motor stimulant effects elicited by DAMGO in the ventral pallidum.
  • The findings highlight a critical role for D1 receptor signaling in opioid-mediated motor control within the VP.

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