5-HT2 and 3 receptor antagonists suppress the response of rat type I slowly adapting mechanoreceptor: an in vitro study

• Published in: Brain research Vol. 969; no. 1; pp. 230 - 236
• Main Authors: He, Liang, Tuckett, Robert P., English, Kathleen B.
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 18.04.2003; Amsterdam Elsevier; New York, NY
• Subjects: 5-HT; Action Potentials - drug effects; Adaptation, Physiological; Animals; Biological and medical sciences; Female; Free Radical Scavengers - pharmacology; Fundamental and applied biological sciences. Psychology; Ketanserin - pharmacology; Male; Mechanoreceptors - drug effects; Mechanoreceptors - physiology; Merkel cell; Organ Culture Techniques; Physical Stimulation; Rats; Rats, Sprague-Dawley; Ritanserin - pharmacology; Serotonin; Serotonin - pharmacology; Serotonin Antagonists - pharmacology; Skin - blood supply; Skin - innervation; Slowly adapting; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors; Tropanes - pharmacology; Type I mechanoreceptor; Vertebrates: nervous system and sense organs; Sensory systems; Serotonin; Type I mechanoreceptor; 5-HT; Slowly adapting; Merkel cell; Rat; Mechanoreceptor; Rodentia; Serotonin 5-HT; Sensory receptor; 5-HT2 Serotonine receptor; Vertebrata; Mammalia; 5-HT3 Serotonine receptor; Antagonist
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(03)02335-7

Previous experiments have shown an increase in rat type I mechanoreceptor responsiveness during arterial serotonin (5-hydroxytryptamine) infusion and the presence of serotonin immunostaining in Merkel cells. The current findings demonstrate that the 5-HT 2 antagonists ritanserin and ketanserin, as well as the 5-HT 3 antagonist MDL 72222, reduce type I response to a standardized mechanical stimulus in an in vitro skin preparation. In addition, ritanserin blocked the enhancement of type I response produced by 5-HT. These experiments suggest that serotonin is released during mechanical distortion of the Merkel cell membrane and alters action potential generation by the type I ending. In addition, it is possible that serotonin, released from outside the type I complex, influences mechanoreceptor responsiveness. For example, serotonin generated during inflammatory events could enhance type I response to mechanical stimulation and thereby increase symptoms of mechanical allodynia.