2005 Fiscal Year Final Research Report Summary
Investigation of mechanisms mediating pubertal treatment of marihuana-induced psychosis
| Project/Area Number |
16591174
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Fukuoka University |
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Principal Investigator |
EGASHIRA Nobuaki Fukuoka University, Faculty of Pharmaceutical Sciences, Assistant Professor, 薬学部, 助手 (80352269)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Michihiro Fukuoka University, Faculty of Pharmaceutical Sciences, Professor, 薬学部, 教授 (10091331)
NISHIMURA Ryoji Fukuoka University, School of Medicine, Professor, 医学部, 教授 (10122722)
IWASAKI Katsunori Fukuoka University, Faculty of Pharmaceutical Sciences, Associate Professor, 薬学部, 助教授 (10183196)
MISHIMA Kenichi Fukuoka University, Faculty of Pharmaceutical Sciences, Assistant Professor, 薬学部, 助手 (00320309)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Δ^9-Tetrahydrocannabinol / CB_1 cannabinoid receptor / Prepulse inhibition / Psychosis / Pubertal / Sensorimotor gating |
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| Research Abstract |
There is evidence from studies in humans and animals that a vulnerable period for chronic cannabinoid administration exists during certain phases of development. In the present study, we investigated whether the chronic administration of Δ^9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, during development impairs the prepulse inhibition (PPI) of the startle reflex in adult mice. The male ddY mice at 8 weeks of age received 21 injections subcutaneous (s.c.) daily. We examined the effect of chronic THC on the PPI, open-field, rota-rod, catalepsy, plus maze and forced swimming tests. As a result, the PPI was significantly disrupted by chronic pubertal THC treatment at 21 days after chronic injection, and these deficits continued until 56 days after chronic injection. In contrast, chronic THC had no effect on the startle response, motor function such as locomotor activity and catalepsy, anxiety and depression. Thus, THC-induced PPI deficits were not due to change of startle response, motor impairment, anxiety and depression. We therefore conclude that development in mice is a vulnerable period with respect to the adverse effects of THC treatment. Since PPI deficits are among the endophenotypes of schizophrenia, we thus propose the chronic administration of THC during development as an animal model for some aspects of the etiology of schizophrenia.
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