Calcium channel activation and self-biting in mice
Author(s) -
Hyder A. Jinnah,
Silaja Yitta,
Touby Drew,
B. S. Kim,
Jasper E. Visser,
Jeffrey D. Rothstein
Publication year - 1999
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.96.26.15228
Subject(s) - nitrendipine , verapamil , nimodipine , calcium channel , dihydropyridine , agonist , voltage dependent calcium channel , flunarizine , nifedipine , biting , diltiazem , calcium , isradipine , l type calcium channel , pharmacology , bay k8644 , chemistry , endocrinology , medicine , biology , receptor , ecology
The L type calcium channel agonist (+/-)Bay K 8644 has been reported to cause characteristic motor abnormalities in adult mice. The current study shows that administration of this drug can also cause the unusual phenomenon of self-injurious biting, particularly when given to young mice. Self-biting is provoked by injecting small quantities of (+/-)Bay K 8644 directly into the lateral ventricle of the brain, suggesting a central effect of the drug. Similar behaviors can be provoked by administration of another L type calcium channel agonist, FPL 64176. The self-biting provoked by (+/-)Bay K 8644 can be inhibited by pretreating the mice with dihydropyridine L type calcium channel antagonists such as nifedipine, nimodipine, or nitrendipine. However, self-biting is not inhibited by nondihydropyridine antagonists including diltiazem, flunarizine, or verapamil. The known actions of (+/-)Bay K 8644 as an L type calcium channel agonist, the reproduction of similar behavior with another L type calcium channel agonist, and the protection afforded by certain L type calcium channel antagonists implicate calcium channels in the mediation of the self-biting behavior. This phenomenon provides a model for studying the neurobiology of this unusual behavior.
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