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Calcium channel activation and self-biting in mice
1Department of Neurology, Johns Hopkins Hospital, Baltimore, MD 21287, USA. hjinnah@welch.jhu.edu
Summary
The L type calcium channel agonist (+/-)Bay K 8644 induces self-injurious biting in young mice, suggesting a central nervous system effect. This behavior is mediated by calcium channels and offers a model for neurobiological studies.
Area of Science:
- Neuropharmacology
- Behavioral Neuroscience
- Calcium Channel Research
Background:
- L-type calcium channels play a role in motor functions.
- (+/-)Bay K 8644 is an L-type calcium channel agonist known to cause motor abnormalities.
Purpose of the Study:
- To investigate the effect of L-type calcium channel agonists on self-injurious behavior in mice.
- To explore the role of central calcium channels in mediating self-biting behavior.
Main Methods:
- Administration of L-type calcium channel agonists ((+/-)Bay K 8644, FPL 64176) into the lateral ventricle of young mice.
- Assessment of self-injurious biting behavior.
- Inhibition studies using dihydropyridine and non-dihydropyridine L-type calcium channel antagonists (nifedipine, nimodipine, nitrendipine, diltiazem, flunarizine, verapamil).
Main Results:
- (+/-)Bay K 8644 administration induced self-injurious biting in young mice, indicating a central effect.
- Another L-type calcium channel agonist, FPL 64176, also provoked similar behaviors.
- Dihydropyridine antagonists (nifedipine, nimodipine, nitrendipine) inhibited the self-biting, while non-dihydropyridine antagonists did not.
Conclusions:
- Calcium channels are implicated in the mediation of self-injurious biting behavior.
- The study provides a novel animal model for investigating the neurobiology of self-injurious behavior.
- Selective L-type calcium channel modulation affects complex behaviors beyond motor control.