title: Serotonin regulates voltage-dependent currents in type I(e(A)) and I(i) interneurons of Hermissenda.
abstract: 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.
authors.affiliation: Dept. of Neurobiology and Anatomy, Univ. of Texas Medical School, 6431 Fannin St., Houston, TX 77030, USA.
authors.forename: Nan Ge
authors.initials: NG
authors.lastname: Jin
authors.forename: Terry
authors.initials: T
authors.lastname: Crow
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D051668:Delayed Rectifier Potassium Channels / Q000502:physiology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology*; D049870:Hermissenda / Q000502:physiology*; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology*; D007395:Interneurons / Q000145:classification / Q000166:cytology / Q000502:physiology*; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024661:Potassium Channels, Inwardly Rectifying / Q000502:physiology; D024642:Potassium Channels, Voltage-Gated / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology / Q000502:physiology*; D019789:Tetraethylammonium / Q000494:pharmacology
chemical_list: D051668:Delayed Rectifier Potassium Channels; D026902:Potassium Channel Blockers; D024661:Potassium Channels, Inwardly Rectifying; D024642:Potassium Channels, Voltage-Gated; D012701:Serotonin; D019789:Tetraethylammonium; D015761:4-Aminopyridine