Serotonin reduces a voltage-dependent transient outward potassium current and enhances excitability of cerebellar Purkinje cells

• Published in: Brain research Vol. 571; no. 2; p. 345
• Main Authors: Wang, Y, Strahlendorf, J C, Strahlendorf, H K
• Format: Journal Article
• Language: English
• Published: Netherlands 07-02-1992
• Subjects: 4-Aminopyridine - pharmacology; Animals; Cerebellum - physiology; Cesium - pharmacology; Dose-Response Relationship, Drug; Electric Stimulation; In Vitro Techniques; Membrane Potentials - drug effects; Nickel - pharmacology; Potassium Channels - drug effects; Potassium Channels - physiology; Purkinje Cells - drug effects; Purkinje Cells - physiology; Rats; Serotonin - pharmacology; Tetraethylammonium; Tetraethylammonium Compounds - pharmacology; Tetrodotoxin - pharmacology
• ISSN: 0006-8993
• DOI: 10.1016/0006-8993(92)90675-Y

Utilizing current-clamp and single electrode voltage-clamp techniques we have studied the actions of serotonin (5-HT) on a transient outward voltage-dependent potassium current in adult rat Purkinje cells (PCs) in vitro. Under voltage-clamp, bath-applied 5-HT (10 nM-100 microM) reversibly depressed a transient outward potassium current in a dose-dependent manner in 24 of 26 neurons. This depression was apparent at all test command voltages. In current clamp, with normal bathing medium, 5-HT decreased the latency to first spike firing and increased the number of spikes in response to depolarization. Similar effects were evident when 4-aminopyridine was applied. In bathing medium containing TTX, Cs+ and Ni2+ to block voltage-activated currents, 5-HT increased the trajectory of the electrotonic membrane response elicited by depolarizing current injection. Enhanced responsiveness of PCs by 5-HT was not related to changes in membrane potential or input resistance. These experiments indicate that one mechanism by which 5-HT can increase the excitability of PCs is via reduction of a transient outward current.