title: Involvement of opioid system in cognitive deficits induced by ∆⁹-tetrahydrocannabinol in rats.
abstract: BACKGROUND
  Cannabis is a widely used illicit substance. ∆(9)-Tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to induce cognitive deficits that closely resemble the impairment observed in schizophrenic patients. We previously reported that THC (6 mg/kg) impairs spatial memory in the eight-arm radial maze, and that this memory disturbance was reversed by the cannabinoid CB(1) receptor antagonist rimonabant (0.1 mg/kg), suggesting that the effect of THC is mediated through cannabinoid CB(1) receptors.
  
  
  OBJECTIVE
  The present study was designed to examine the possible involvement of opioid receptors in the THC-induced impairment of spatial memory.
  
  
  METHODS
  The effects of treatment with the nonselective opioid receptor antagonist naloxone (0.3 and 1 mg/kg), the μ-opioid receptor antagonist β-funaltrexamine (0.3 and 1 mg/kg), the δ-opioid receptor antagonist naltrindole (1 and 3 mg/kg), and the κ-opioid receptor antagonist nor-binaltorphimine (0.03 and 0.1 mg/kg) on the impairment of spatial memory induced by THC were evaluated using the eight-arm radial maze.
  
  
  RESULTS
  The nonselective opioid receptor antagonist naloxone, the μ-opioid receptor antagonist β-funaltrexamine, and the κ-opioid receptor antagonist nor-binaltorphimine, but not the δ-opioid receptor antagonist naltrindole, attenuated THC-induced cognitive deficits, suggesting an involvement of μ- and κ-opioid receptors in this behavioral response.
  
  
  CONCLUSIONS
  These results demonstrate that the endogenous opioid system is involved in the regulation of the acute short-term and working memory deficits induced by cannabis.
authors.affiliation: Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka 814-0180, Japan. n-egashi@pharm.med.kyushu-u.ac.jp
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Egashira
authors.forename: Naomi
authors.initials: N
authors.lastname: Manome
authors.forename: Kenichi
authors.initials: K
authors.lastname: Mishima
authors.forename: Katsunori
authors.initials: K
authors.lastname: Iwasaki
authors.forename: Ryozo
authors.initials: R
authors.lastname: Oishi
authors.forename: Michihiro
authors.initials: M
authors.lastname: Fujiwara
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D003072:Cognition Disorders / Q000139:chemically induced*; D013759:Dronabinol / Q000633:toxicity*; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D008569:Memory Disorders / Q000139:chemically induced*; D009292:Narcotic Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011957:Receptors, Opioid / Q000187:drug effects* / Q000378:metabolism; D017473:Receptors, Opioid, kappa / Q000187:drug effects / Q000378:metabolism; D017450:Receptors, Opioid, mu / Q000187:drug effects / Q000378:metabolism
chemical_list: D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; D013759:Dronabinol