Enkephalinergic and GABAergic modulation of motor activity in the ventral pallidum.
Injection of the mu-opioid receptor agonist, Tyr-D-Ala-Gly-NMe-Phe-Gly-ol (DAMGO), produced a dose-dependent increase in horizontal motor activity after injection into the ventral pallidum or substantia innominata (VP/SI) of the rat. INjection of the delta-opioid receptor agonist, [D-Pen2,5]-enkephalin, produced a markedly reduced motor stimulant action, as did injection of DAMGO outside the VP/SI. Injection of the GABAA receptor antagonist, bicuculline, or the antagonist of the GABAA chloride channel, picrotoxin, also produced a dose-related elevation in horizontal motor activity. In contrast, the GABAB receptor antagonist, phaclofen, was without effect. The motor stimulant actions of both DAMGO and picrotoxin were attenuated by pretreatment in the VP/SI with the GABAA receptor agonist, muscimol. In contrast, pretreatment with the opioid receptor antagonist, naloxone, abolished only the actions of DAMGO on motor activity. These data demonstrate that motor activity can be regulated in the VP/SI by mu-opioid and GABAA neurotransmission, and that the response to mu-opioids can be modulated by GABAergic transmission.[1]References
- Enkephalinergic and GABAergic modulation of motor activity in the ventral pallidum. Austin, M.C., Kalivas, P.W. J. Pharmacol. Exp. Ther. (1990) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg