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Centrally administered opioid peptides stimulate saccharin intake in nondeprived rats

Authors :
University of Michigan, Department of Psychiatry University Hospital, 8D8806, Box 0116, Ann Arbor, MI 48109-0116, USA
Gosnell, Blake A.
Majchrzak, Mark J.
University of Michigan, Department of Psychiatry University Hospital, 8D8806, Box 0116, Ann Arbor, MI 48109-0116, USA
Gosnell, Blake A.
Majchrzak, Mark J.
Publication Year :
2006

Abstract

Endogenous opioid peptides are thought to play a role in mediating the pleasurable or rewarding aspects of the ingestion of certain foods and liquids. We therefore measured the effects of central administration of selective opioid agonists and naloxone on the intake of two concentrations of saccharin solution. All tests were performed on nondeprived rats, such that the taste of the solutions provided the primary incentive to consume. Intracerebroventricular (ICV) administration of the selective mu agonist [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAGO) and the selective delta agonist Tyr-D-Thr-Gly-Phe-Leu-Thr (DTLET) (3 nmol) increased intake of a 0.15% saccharin solution by approximately 10 ml over 3 hr. Water was available simultaneously, but intake was minimal. The selective kappa agonist U-50,488H did not increase intake of the saccharin solution. Naloxone (30 and 100 [mu]g, ICV) caused a 44% reduction in saccharin solution intake in the first hour; two- and three-hour cumulative intakes were not different from control. DAGO and DTLET were also tested when rats were given a weaker saccharin solution (0.006%) along with water. Both agonists caused small increases in saccharin and water intake, but the increases above baseline were much smaller than those observed with the more palatable 0.15% saccharin solution. These results are consistent with reports by others which suggest that endogenous opioids influence taste preferences or palatability. Further, they indicate a role for central mu and delta opioid receptors in the mediation of this influence.

Details

Database :
OAIster
Notes :
En_US
Publication Type :
Electronic Resource
Accession number :
edsoai.ocn894058260
Document Type :
Electronic Resource