Serotonin regulates voltage-dependent currents in type I(e(A)) and I(i) interneurons of Hermissenda

• Published in: Journal of neurophysiology Vol. 106; no. 5; pp. 2557 - 2569
• Main Authors: Jin, Nan Ge, Crow, Terry
• Format: Journal Article
• Language: English
• Published: United States 01.11.2011
• Subjects: 4-Aminopyridine - pharmacology; Animals; Delayed Rectifier Potassium Channels - physiology; Excitatory Postsynaptic Potentials - drug effects; Excitatory Postsynaptic Potentials - physiology; Hermissenda - physiology; Inhibitory Postsynaptic Potentials - drug effects; Inhibitory Postsynaptic Potentials - physiology; Interneurons - classification; Interneurons - cytology; Interneurons - physiology; Patch-Clamp Techniques; Potassium Channel Blockers - pharmacology; Potassium Channels, Inwardly Rectifying - physiology; Potassium Channels, Voltage-Gated - physiology; Serotonin - pharmacology; Serotonin - physiology; Tetraethylammonium - pharmacology
• ISSN: 1522-1598
• DOI: 10.1152/jn.00550.2011

Serotonin (5-HT) has both direct and modulatory actions on central neurons contributing to behavioral arousal and cellular-synaptic plasticity in diverse species. In Hermissenda, 5-HT produces changes in intrinsic excitability of different types of identified interneurons in the circumesophageal nervous system. Using whole cell patch-clamp techniques we have examined membrane conductance changes produced by 5-HT that contribute to intrinsic excitability in two identified classes of interneurons, types I(i) and I(eA). Whole cell currents were examined before and after 5-HT application to the isolated nervous system. A 4-aminopyridine-sensitive transient outward K(+) current [I(K(A))], a tetraethylammonium-sensitive delayed rectifier K(+) current [I(K(V))], an inward rectifier K(+) current [I(K(IR))], and a hyperpolarization-activated current (I(h)) were characterized. 5-HT decreased the amplitude of I(K(A)) and I(K(V)) in both type I(i) and I(eA) interneurons. However, differences in 5-HT's effects on the activation-inactivation kinetics were observed in different types of interneurons. 5-HT produced a depolarizing shift in the activation curve of I(K(V)) and a hyperpolarizing shift in the inactivation curve of I(K(A)) in type I(i) interneurons. In contrast, 5-HT produced a depolarizing shift in the activation curve and a hyperpolarizing shift in the inactivation curve of both I(K(V)) and I(K(A)) in type I(eA) interneurons. In addition, 5-HT decreased the amplitude of I(K(IR)) in type I(i) interneurons and increased the amplitude of I(h) in type I(eA) interneurons. These results indicate that 5-HT-dependent changes in I(K(A)), I(K(V)), I(K(IR)), and I(h) contribute to multiple mechanisms that synergistically support modulation of increased intrinsic excitability associated with different functional classes of identified type I interneurons.