Effects of Tandospirone, a 5-HT1A Agonistic Anxiolytic Agent, on Haloperidol-Induced Catalepsy and Forebrain Fos Expression in Mice
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- Ohno Yukihiro
- Laboratory of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan
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- Shimizu Saki
- Laboratory of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan
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- Imaki Junta
- Laboratory of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan
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We studied the effects of tandospirone, a 5-HT1A agonistic anxiolytic agent, on haloperidol-induced catalepsy and forebrain Fos expression in mice. Haloperidol (0.5 mg/kg, i.p.) markedly increased the catalepsy time and enhanced Fos expression in the shell (AcS) and core (AcC) regions of the nucleus accumbens, the dorsolateral striatum (dlST), and the lateral septal nucleus (LSN). Tandospirone (0.1 – 1 mg/kg, s.c.) significantly alleviated haloperidol-induced catalepsy in a dose-dependent manner, which was antagonized by WAY-100135 (a selective 5-HT1A antagonist). The anticataleptic dose of tandospirone (1 mg/kg, s.c.) significantly reduced haloperidol-induced Fos expression in the dlST. This inhibition by tandospirone was regionally specific, and it failed to affect haloperidol-induced Fos expression either in the AcS, AcC, or LSN. In addition, the reversal of haloperidol-induced striatal Fos expression by tandospirone was antagonized by WAY-100135. These results support the notion that stimulation of 5-HT1A receptors region-specifically counteracts the D2-blocking actions of haloperidol in the striatum, which may account for the ameliorative effects of 5-HT1A agonists on antipsychotic-associated extrapyramidal disorders.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 109 (4), 593-599, 2009
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680157324672
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- NII論文ID
- 10025736020
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BD1MXlsFSgu7c%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 10209803
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- PubMed
- 19352073
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可