Microinjection of sigma ligands into cranial nerve nuclei produces vacuous chewing in rats.
Many typical neuroleptics carry a high risk for producing motor side effects in humans, and have significant affinities for sigma (sigma) receptors. Sigma receptors are densely concentrated in cranial nerve nuclei that comprise the final common pathways for lingual, facial and masticatory movements; thus, they may serve as important substrates for some of the unwanted movements that can accompany neuroleptic treatment. Therefore, the purpose of this study was to evaluate whether microinjection of sigma ligands into the facial nucleus or spinal trigeminal nucleus, oralis would cause orofacial dyskinesias, and whether these effects could be attenuated with sigma receptor antagonists. Microinjection of the high affinity sigma ligands, di-o-tolylguanidine or haloperidol (0-10 nmol/0.5 microl), produced a marked increase in vacuous chewing and facial tremors in rats, while coadministration of the functional sigma antagonists, BD1047 or BD1063 (5 nmol), greatly attenuated these drug-induced movements. Sulpiride and clozapine (10 nmol/0.5 microl), sigma inactive/dopamine active atypical antipsychotic drugs with a much reduced risk for producing motor side effects in humans, were unable to elicit orofacial dyskinesias when microinjected into the facial or spinal trigeminal nucleus, oralis. These studies indicate that sigma receptors may contribute to some forms of motor side effects resulting from antipsychotic drug treatment.[1]References
- Microinjection of sigma ligands into cranial nerve nuclei produces vacuous chewing in rats. Tran, T.T., de Costa, B.R., Matsumoto, R.R. Psychopharmacology (Berl.) (1998) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
