Please use this identifier to cite or link to this item: https://www.um.edu.mt/library/oar/handle/123456789/22606
Title: 5-HT2 receptors-mediated modulation of voltage-gated K+ channels and neurophysiopathological correlates
Authors: D'Adamo, Maria Cristina
Servettini, Ilenio
Guglielmi, Luca
Matteo, Vincenzo di
Maio, Roberto di
Di Giovanni, Giuseppe
Pessia, Mauro
Keywords: Receptor, Serotonin, 5-HT2C
Receptor, Serotonin, 5-HT2A
Kv1.1 potassium channel
Kv1.2 potassium channel
Issue Date: 2013
Publisher: Springer
Citation: D'Adamo, M. C., Servettini, I., Guglielmi, L., Di Matteo, V., Di Maio, R., Di Giovanni, G., & Pessia, M. (2013). 5-HT2 receptors-mediated modulation of voltage-gated K+ channels and neurophysiopathological correlates. Experimental Brain Research, 230(4), 453-462.
Abstract: The activity of voltage-gated K(+) channels (Kv) can be dynamically modulated by several events, including neurotransmitter stimulated biochemical cascades mediated by G protein-coupled receptors such as 5-HT2 receptors (5-HT2Rs). Activation of 5-HT2A/CR inhibits the Shaker-like K(+) channels Kv1.1 and Kv1.2, and this modulation involves the dual coordination of both RPTPĪ± and distinct tyrosine kinases coupled to this receptor; 5-HT2Rs-mediated modulation of Kv channels controls glutamate release onto prefrontal cortex neurons that might play critical roles in neurophysiological, neurological, and psychiatric conditions. Noticeably, hallucinogens modulate Kv channel activity, acting at 5-HT2R. Hence, comprehensive knowledge of 5-HT2R signaling through modulation of distinct K(+) channels is a pivotal step in the direction that will enable scientists to discover novel 5-HT functions and dysfunctions in the brain and to identify original therapeutic targets.
URI: https://www.um.edu.mt/library/oar//handle/123456789/22606
Appears in Collections:Scholarly Works - FacM&SPB

Files in This Item:
File Description SizeFormat 
DAdamo et al EBR 2013.pdf548.72 kBAdobe PDFView/Open


Items in OAR@UM are protected by copyright, with all rights reserved, unless otherwise indicated.