Abstract:
:The hyperphagic properties of insulin (10 U/kg, s.c.) were transiently (2h) and dose-dependently inhibited (30%) by central pretreatment with naltrexone (20-50 micrograms, i.c.v.). The irreversible mu opioid antagonist, beta-funaltrexamine (B-FNA, 20 micrograms, i.c.v.) significantly inhibited insulin hyperphagia by 28-54% over the 6-h time course. In contrast, insulin hyperphagia was only transiently (2 h) inhibited (27-30%) by either the irreversible mu 1 antagonist, naloxonazine (50 micrograms, i.c.v.) or the selective kappa antagonist, nor-binaltorphamine (NorBNI, 20 micrograms, i.c.v.). The delta-antagonistic actions of [D-Ala2, Leu5, Cys6]-enkephalin (DALCE, 40 micrograms, i.c.v.) failed to affect insulin hyperphagia. These data suggest that the mu 2 opioid receptor subtype modulates insulin hyperphagia.
journal_name
Brain Resjournal_title
Brain researchauthors
Beczkowska IW,Bodnar RJdoi
10.1016/0006-8993(91)90977-4subject
Has Abstractpub_date
1991-05-03 00:00:00pages
315-8issue
2eissn
0006-8993issn
1872-6240pii
0006-8993(91)90977-4journal_volume
547pub_type
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