Involvement of opioid system in cognitive deficits induced by ∆⁹-tetrahydrocannabinol in rats.
Nobuaki Egashira, Naomi Manome, Kenichi Mishima, Katsunori Iwasaki, Ryozo Oishi, Michihiro Fujiwara
Psychopharmacology February 2012 DOI: 10.1007/s00213-011-2442-x (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational cohort Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | THC Naloxone β-funaltrexamine Naltrindole Nor-binaltorphimine |
| Dose | THC 6 mg/kg; naloxone 0.3 and 1 mg/kg; β-funaltrexamine 0.3 and 1 mg/kg; naltrindole 1 and 3 mg/kg; nor-binaltorphimine 0.03 and 0.1 mg/kg |
| Topics | Cannabis |
| Key findings | Naloxone, β-funaltrexamine, and nor-binaltorphimine, but not naltrindole, attenuated THC-induced spatial memory impairment, indicating that μ- and κ-opioid receptors mediate these deficits. |
Abstract
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. The present study was designed to examine the possible involvement of opioid receptors in the THC-induced impairment of spatial memory. 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. 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. 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.