5-HT2 receptors-mediated modulation of voltage-gated K+ channels and neurophysiopathological correlates.
Maria Cristina D'Adamo, Ilenio Servettini, Luca Guglielmi, Vincenzo Di Matteo, Roberto Di Maio, Giuseppe Di Giovanni, Mauro Pessia
Experimental Brain Research October 2013 DOI: 10.1007/s00221-013-3555-8 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Review Peer reviewed |
|---|---|
| Topics | Serotonin |
| Key findings | The authors propose that 5-HT2 receptor signaling modulates Kv1.1 and Kv1.2 potassium channels through coordinated action of RPTPα and receptor-coupled tyrosine kinases, and that this modulation controls glutamate release onto prefrontal cortex neurons. They argue that hallucinogens act on this pathway and that clarifying it could identify new therapeutic targets. |
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 RPTPα 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.
Comparable studies
Other narrative reviews on serotonin, most cited first.
Citations in the library
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