Role of vasopressin V1a receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice

Nobuaki Egashira, Emi Koushi, Takayuki Myose, Akito Tanoue, Kenichi Mishima, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki

研究成果: ジャーナルへの寄稿学術誌査読


Rationale: Cannabis is a widely used illicit substance. ∆9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to cause catalepsy in rodents. Recent studies have shown that vasopressin V1a and V1b receptors are widely distributed in the central nervous system and are capable of influencing a wide variety of brain functions such as social behavior, emotionality, and learning and memory. Objectives: The present study was designed to examine the possible involvement of V1a and V1b receptors in THC-induced catalepsy-like immobilization. Methods: The induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a receptor knockout (V1aRKO), and V1b receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine1A receptor antagonist WAY100635 (0.1 mg/kg, i.p.) on THC-induced catalepsy was also evaluated in V1aRKO mice. Moreover, the effects of the V1a receptor antagonist VMAX-357 and the V1b receptor antagonist ORG-52186 on THC-induced catalepsy were evaluated in ddY mice. Results: THC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice. Conclusions: These findings suggest that V1a receptor regulates THC-induced catalepsy-like immobilization.

出版ステータス出版済み - 12月 1 2017

!!!All Science Journal Classification (ASJC) codes

  • 薬理学


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