Elsevier

Brain Research

Volume 436, Issue 1, 8 December 1987, Pages 169-172
Brain Research

Short communication
Place preference conditioning reveals the involvement of D1-dopamine receptors in the motivational properties of μ- and κ-opioid agonists

https://doi.org/10.1016/0006-8993(87)91571-XGet rights and content

Abstract

The role of D1 dopamine receptors in mediating the motivational properties of opioid agonists was investigated by use of place preference conditioning. Administration of the D1 receptor antagonist SCH 23390 (0.001–0.5 mg/kg) or the κ-opioid receptor agonist U-69593 (0.16 mg/kg) produced conditioned place aversions. In contrast, the μ-opioid agonist, morphine (3.0 mg/kg) was appetitively reinforcing. Chronic infusion of SCH 23390 (1.0 mg/kg/day) during conditioning abolished the effects of both opioid agonists. These data demonstrate the specific involvement of D1 receptors in the motivational properties of μ- and κ-opioid agonists and suggest that dopaminergic systems are crucial for the expression of both reinforcing and aversive motivational states.

References (21)

There are more references available in the full text version of this article.

Cited by (162)

  • Dopamine D1 and D3 receptor modulators restore morphine analgesia and prevent opioid preference in a model of neuropathic pain

    2019, Neuroscience
    Citation Excerpt :

    Assessment of D1R and reward potential is well established. Our results in a SCI model confirm what was previously observed for D1R antagonists; they block the induction of conditioned place preference for many drugs of abuse including morphine (Shippenberg and Herz, 1987; Acquas et al., 1989; Nakajima and O'Regan, 1991; Acquas and Di Chiara, 1994). Despite, the ability of D1R agonists to block morphine reward being well established, the underlying mechanism for D1R and D3R effects on morphine reward is currently unknown.

  • Understanding opioid reward

    2015, Trends in Neurosciences
    Citation Excerpt :

    The canonical model of opioid reward asserts that the critical dopaminergic terminal region is the ventral striatum. Indeed, dopamine D1 receptor antagonists microinjected into the NAc can reduce MOP receptor agonist reinforcement [89]. However, recent evidence suggests that dopamine can be released in the striatum independent of increases in VTA dopamine neuron activity: first, VTA GABA neurons that project to the NAc synapse onto cholinergic interneurons [39]; second, cholinergic interneuron activation in the NAc can stimulate dopamine release through nicotinic acetylcholine receptors on the striatal terminals of dopamine neurons [90,91].

View all citing articles on Scopus
View full text