Serotonin regulates voltage-dependent currents in type Ie(A)and Iiinterneurons ofHermissenda

Author:

Jin Nan Ge1,Crow Terry1

Affiliation:

1. Department of Neurobiology and Anatomy, University of Texas Medical School, Houston, Texas

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 Iiand IeA. Whole cell currents were examined before and after 5-HT application to the isolated nervous system. A 4-aminopyridine-sensitive transient outward K+current [ IK(A)], a tetraethylammonium-sensitive delayed rectifier K+current [ IK(V)], an inward rectifier K+current [ IK(IR)], and a hyperpolarization-activated current ( Ih) were characterized. 5-HT decreased the amplitude of IK(A)and IK(V)in both type Iiand IeAinterneurons. 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 IK(V)and a hyperpolarizing shift in the inactivation curve of IK(A)in type Iiinterneurons. In contrast, 5-HT produced a depolarizing shift in the activation curve and a hyperpolarizing shift in the inactivation curve of both IK(V)and IK(A)in type IeAinterneurons. In addition, 5-HT decreased the amplitude of IK(IR)in type Iiinterneurons and increased the amplitude of Ihin type IeAinterneurons. These results indicate that 5-HT-dependent changes in IK(A), IK(V), IK(IR), and Ihcontribute to multiple mechanisms that synergistically support modulation of increased intrinsic excitability associated with different functional classes of identified type I interneurons.

Publisher

American Physiological Society

Subject

Physiology,General Neuroscience

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