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

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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.

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Acknowledgements

We thank Otsuka Pharmaceutical Co., Ltd. for generously donating the VMAX-357 and ORG-52186 used in this study. All animal experiments were performed in accordance with current Japanese legislation regarding the use of laboratory animals.

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Authors and Affiliations

  1. Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan

    Nobuaki Egashira, Emi Koushi & Katsunori Iwasaki

  2. Department of Pharmacy, Kyushu University Hospital, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan

    Nobuaki Egashira

  3. Department of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan

    Takayuki Myose & Kenichi Mishima

  4. Department of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo, 157-8535, Japan

    Akito Tanoue

  5. Department of Pharmacognosy, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan

    Ryota Tsuchihashi & Junei Kinjo

  6. Department of Pharmacognosy, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan

    Hiroyuki Tanaka & Satoshi Morimoto

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  1. Nobuaki Egashira
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  2. Emi Koushi
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  3. Takayuki Myose
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  10. Katsunori Iwasaki
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Correspondence to Nobuaki Egashira.

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All animal care and use procedures were performed in compliance with the regulations established by the Experimental Animal Care and Use Committee of Fukuoka University, which are in accordance with the universal principles of laboratory animal care.

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The authors declare that they have no conflict of interest.

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Egashira, N., Koushi, E., Myose, T. et al. Role of vasopressin V1a receptor in ∆9-tetrahydrocannabinol-induced cataleptic immobilization in mice. Psychopharmacology 234, 3475–3483 (2017). https://doi.org/10.1007/s00213-017-4735-1

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  • DOI: https://doi.org/10.1007/s00213-017-4735-1

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