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Characterization of the effects of (±)‐meptazinol, its individual enantiomers and N‐methyl meptazinol on food consumption in the rat
Author(s) -
Jackson Helen C.,
Sewell R.D.E.
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb10252.x
Subject(s) - levorphanol , naltrexone , chemistry , opioid , morphine , pharmacology , antagonist , narcotic antagonist , opioid receptor , (+) naloxone , receptor , medicine , biochemistry
1 Both (±)‐meptazinol (2 mg kg −1 ) and levorphanol (1 mg kg −1 ) produced hyperphagia over a 4 h period after intraperitoneal injection in free feeding rats during the daylight phase. 2 The individual (+)‐ and (−)‐enantiomers of meptazinol (2 mg kg −1 i.p.) induced comparable increases in cumulative food intake. 3 N‐methyl meptazinol (2–10 mg kg −1 i.p.), the quaternary analogue of meptazinol, produced no modification of food intake though it increased food consumption when injected intracerebroventricularly (10–100 μg per animal). 4 Meptazinol and levorphanol hyperphagia was abolished by 1 mg kg −1 doses (i.p.) of the opioid antagonists naltrexone, naloxonazine and (−)‐Mr 1452 but not by its (+)‐enantiomer Mr 1453 which is not effective as an opioid antagonist. 5 Intracerebroventricular administration of the δ‐opioid receptor antagonist ICI 154,129 (10 μg per animal) suppressed meptazinol but not levorphanol hyperphagia. 6 It was concluded that meptazinol produces centrally mediated stereospecifically reversible hyperphagia through a μ‐opioid receptor mechanism common to levorphanol, and also through δ‐opioid receptor mechanism(s).