Motor hypoactivity induced by neurotensin and related peptides in mice.
The tridecapeptide neurotensin (NT) induces a variety of behavioral changes in animals. The present study characterizes the behavioral hypoactivity observed after intracerebroventricular (ICV) injection in mice. At doses higher than 25 ng, NT induced a reduction of general motor activity and increases in immobility which lasted for about one hour. The NT-related amphibian skin peptide xenopsin was about 70-fold more potent than NT itself. After repeated NT-injections, tolerance developed within 2-4 days and disappeared within 2-4 days after cessation of the treatment. The motor hypoactivity induced by NT was not attenuated by pretreatment with naloxone (5 mg/kg, SC). Furthermore, amphetamine-induced locomotor activity was not blocked by NT or xenopsin. These results suggest that the NT-effect is not mediated by a stimulation of opioid mechanisms or attenuation of dopamine-mediated events.
D000661:Amphetamine / Q000494:pharmacology; D000818:Animals; D004347:Drug Interactions; D004361:Drug Tolerance; D006120:Grooming / Q000187:drug effects; D007276:Injections, Intraventricular; D008297:Male; D051379:Mice; D009043:Motor Activity / Q000187:drug effects*; D009270:Naloxone / Q000494:pharmacology; D009496:Neurotensin / Q000031:analogs & derivatives / Q000494:pharmacology*; D009842:Oligopeptides / Q000494:pharmacology; D010455:Peptides; D013329:Structure-Activity Relationship; D029867:Xenopus Proteins
D009842:Oligopeptides; D010455:Peptides; D029867:Xenopus Proteins; D009270:Naloxone; D009496:Neurotensin; C016832:xenopsin; D000661:Amphetamine