Role of 5-HT3 receptors in the mechanisms of central pain syndrome.
Electrophysiological and behavioral studies showed that spinal 5-HT3 receptors are involved in the regulation of pain sensitivity in rats. Intrathecal administration of the 5-HT3 receptor antagonist tropine (200 microg) produced allodynia, reduced the threshold, decreased the latency, and increased the number of spikes in the late component of the nociceptive flexion reflex. Intrathecal administration of 5-HT3 receptor agonist quipazine (200 mg) abolished nociceptive flexion reflex and alleviated spinal pain syndrome produced by impairment of GABAergic inhibition in the lumbar spinal segments. Our results indicate that spinal 5-HT3 receptors are involved in the modulation of pain sensitivity: activation of these receptors inhibits nociceptive reactions, while blockade of 5-HT3 receptors potentiates the nociceptive response via modulation of excitability of GABAergic interneurons.[1]References
- Role of 5-HT3 receptors in the mechanisms of central pain syndrome. Kukushkin, M.L., Igon'kina, S.I. Bull. Exp. Biol. Med. (2003) [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