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Nucleus-accumbens opiate-dopamine interactions and locomotor activation in the rat - evidence for a presynaptic locus

Academic Article
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Overview

authors

  • Swerdlow, N. R.
  • Amalric, M.
  • Koob, George

publication date

  • April 1987

journal

  • Pharmacology, Biochemistry and Behavior  Journal

abstract

  • Locomotor activation produced by the indirect dopamine (DA) agonist amphetamine is reversed by the opiate-receptor antagonist naloxone. Since amphetamine-stimulated locomotion results from the release of DA within the nucleus accumbens (N.Acc.), it is possible that these effects of naloxone result either from a decrease in the pre-synaptic release of DA within the N.Acc. or from a disruption of the effects of DA at, or distal to, the post-synaptic DA receptor. In the present study, we investigated the effects of naloxone on the locomotor-activating properties of dopamine injected directly into the nucleus accumbens. Naloxone (0-2 mg/kg) had no significant effect of DA-stimulated locomotion; the lowest dose of naloxone tested (0.5 mg/kg) was shown to significantly disrupt the locomotor activation produced by amphetamine (0.5 mg/kg). In separate animals, very high doses of naloxone (5.0 mg/kg) had no significant effect on locomotor activation produced by the DA receptor agonist apomorphine in rats following 6-hydroxydopamine (6OHDA) denervation of the N.Acc. These results indicate that naloxone must disrupt amphetamine-stimulated locomotion through its action presynaptic to N.Acc. DA receptors.

subject areas

  • Amphetamine
  • Animals
  • Apomorphine
  • Dopamine
  • Hydroxydopamines
  • Male
  • Motor Activity
  • Naloxone
  • Nucleus Accumbens
  • Oxidopamine
  • Rats
  • Rats, Inbred Strains
  • Septal Nuclei
  • Synapses
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Identity

International Standard Serial Number (ISSN)

  • 0091-3057

Digital Object Identifier (DOI)

  • 10.1016/0091-3057(87)90609-5

PubMed ID

  • 3110795
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Additional Document Info

start page

  • 765

end page

  • 769

volume

  • 26

issue

  • 4

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