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記事

抄録

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.

元の言語英語
ページ(範囲)3475-3483
ページ数9
ジャーナルPsychopharmacology
234
発行部数23-24
DOI
出版物ステータス出版済み - 12 1 2017

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Catalepsy
Vasopressin Receptors
Dronabinol
Immobilization
Knockout Mice
Haloperidol
Cannabis
Social Behavior
Rodentia
Central Nervous System

All Science Journal Classification (ASJC) codes

  • Pharmacology

これを引用

Egashira, N., Koushi, E., Myose, T., Tanoue, A., Mishima, K., Tsuchihashi, R., ... Iwasaki, K. (2017). Role of vasopressin V1a receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice. Psychopharmacology, 234(23-24), 3475-3483. https://doi.org/10.1007/s00213-017-4735-1

Role of vasopressin V1a receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice. / Egashira, Nobuaki; Koushi, Emi; Myose, Takayuki; Tanoue, Akito; Mishima, Kenichi; Tsuchihashi, Ryota; Kinjo, Junei; Tanaka, Hiroyuki; Morimoto, Satoshi; Iwasaki, Katsunori.

:: Psychopharmacology, 巻 234, 番号 23-24, 01.12.2017, p. 3475-3483.

研究成果: ジャーナルへの寄稿記事

Egashira, N, Koushi, E, Myose, T, Tanoue, A, Mishima, K, Tsuchihashi, R, Kinjo, J, Tanaka, H, Morimoto, S & Iwasaki, K 2017, 'Role of vasopressin V1a receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice', Psychopharmacology, 巻. 234, 番号 23-24, pp. 3475-3483. https://doi.org/10.1007/s00213-017-4735-1
Egashira, Nobuaki ; Koushi, Emi ; Myose, Takayuki ; Tanoue, Akito ; Mishima, Kenichi ; Tsuchihashi, Ryota ; Kinjo, Junei ; Tanaka, Hiroyuki ; Morimoto, Satoshi ; Iwasaki, Katsunori. / Role of vasopressin V1a receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice. :: Psychopharmacology. 2017 ; 巻 234, 番号 23-24. pp. 3475-3483.
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abstract = "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.",
author = "Nobuaki Egashira and Emi Koushi and Takayuki Myose and Akito Tanoue and Kenichi Mishima and Ryota Tsuchihashi and Junei Kinjo and Hiroyuki Tanaka and Satoshi Morimoto and Katsunori Iwasaki",
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T1 - Role of vasopressin V1a receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice

AU - Egashira, Nobuaki

AU - Koushi, Emi

AU - Myose, Takayuki

AU - Tanoue, Akito

AU - Mishima, Kenichi

AU - Tsuchihashi, Ryota

AU - Kinjo, Junei

AU - Tanaka, Hiroyuki

AU - Morimoto, Satoshi

AU - Iwasaki, Katsunori

PY - 2017/12/1

Y1 - 2017/12/1

N2 - 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.

AB - 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.

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