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Start Over Author "Amano, Taiju" Publisher japanese pharmacological society
17 results on '"Amano, Taiju"'

5. Diverse intracellular signaling pathways mediate the effects of neurotensin on the excitability of type II neurons in the rat dorsolateral bed nucleus of the stria terminalis

Author

Kaneko, Tomoyuki, Hara, Ryuto, Amano, Taiju, Minami, Masabumi, Kaneko, Tomoyuki, Hara, Ryuto, Amano, Taiju, and Minami, Masabumi

Abstract

We examined the effects of neurotensin (NTS) on the excitability of type II neurons in the rat dorsolateral bed nucleus of the stria terminalis (dlBNST) using whole-cell patch-clamp electrophysiology. Bath-application of NTS depolarized type II dlBNST neurons. Analyses of the steady-state I-V relationships implied that the depolarizing effect of NTS is due to potassium conductance blocking. The depolarizing effect of NTS was abolished in the presence of a PLC inhibitor, but not affected by a protein kinase C inhibitor. In the presence of a CaMKII inhibitor, NTS showed depolarizing effects via the increase in nonselective cation conductance in addition to the decrease in potassium conductance. Unexpectedly, in the presence of a PKA inhibitor, NTS hyperpolarized type II dlBNST neurons. These results reveal that diverse signaling pathways mediate the effects of NTS on the excitability of type II dlBNST neurons. The elevation of intracellular Ca2+ levels via the inositol phosphate-mediated signaling activates both Ca2+-dependent adenylate cyclase (AC) and CaMKII. Activation of the AC-cAMP-PKA pathway exerts depolarizing effects on type II dlBNST neurons by decreasing potassium conductance and increasing non-selective cation conductance, whereas activation of the CaMKII pathway exerts hyperpolarizing effects on dlBNST neurons by decreasing non-selective cation conductance.

Published
2021

17. Diverse intracellular signaling pathways mediate the effects of neurotensin on the excitability of type II neurons in the rat dorsolateral bed nucleus of the stria terminalis.

Author

Kaneko T, Hara R, Amano T, and Minami M

Subjects
Adenylyl Cyclases metabolism, Animals, Calcium metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2 antagonists & inhibitors, Calcium-Calmodulin-Dependent Protein Kinase Type 2 metabolism, Cells, Cultured, Male, Patch-Clamp Techniques methods, Rats, Sprague-Dawley, Rats, Neurons drug effects, Neurons physiology, Neurotensin pharmacology, Septal Nuclei cytology, Signal Transduction physiology, Synaptic Transmission drug effects
Abstract

We examined the effects of neurotensin (NTS) on the excitability of type II neurons in the rat dorsolateral bed nucleus of the stria terminalis (dlBNST) using whole-cell patch-clamp electrophysiology. Bath-application of NTS depolarized type II dlBNST neurons. Analyses of the steady-state I-V relationships implied that the depolarizing effect of NTS is due to potassium conductance blocking. The depolarizing effect of NTS was abolished in the presence of a PLC inhibitor, but not affected by a protein kinase C inhibitor. In the presence of a CaMKII inhibitor, NTS showed depolarizing effects via the increase in non-selective cation conductance in addition to the decrease in potassium conductance. Unexpectedly, in the presence of a PKA inhibitor, NTS hyperpolarized type II dlBNST neurons. These results reveal that diverse signaling pathways mediate the effects of NTS on the excitability of type II dlBNST neurons. The elevation of intracellular Ca 2+ levels via the inositol phosphate-mediated signaling activates both Ca 2+ -dependent adenylate cyclase (AC) and CaMKII. Activation of the AC-cAMP-PKA pathway exerts depolarizing effects on type II dlBNST neurons by decreasing potassium conductance and increasing non-selective cation conductance, whereas activation of the CaMKII pathway exerts hyperpolarizing effects on dlBNST neurons by decreasing non-selective cation conductance., Competing Interests: Declaration of competing interest No competing interest., (Copyright © 2021 The Authors. Production and hosting by Elsevier B.V. All rights reserved.)

Published
2021
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