Inhibition of voltage-gated K+ channel gene expression by the neuropeptide thyrotropin-releasing hormone

Koichi Takimoto, Robert Gealy, Alla F Fomina, James Trimmer, Edwin S. Levitan

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Many neurotransmitters regulate action potential activity in neuronal, endocrine, and cardiac cells by rapidly modulating the gating of K+ channels. Neurotransmitters might also produce prolonged effects on excitability by regulating the expression of K+ channel genes. Here we show that the neuropeptide thyrotropin-releasing hormone (TRH) down-regulates Kv1.5 and Kv2.1 K+ channel mRNAs in clonal pituitary cells. The effect on Kv1.5 mRNA expression does not require protein synthesis and is due to decreased transcription. Immunoblots demonstrate that Kv1.5 and Kv2.1 immunoreactivities are significantly reduced by TRH within 12 hr. The change in channel protein expression is associated with a decrease in voltage-gated K+ currents. Thus, TRH enhances excitability by inhibiting K+ channel gene expression. Neuropeptide regulation of K+ channel gene expression may produce long-term changes in neuronal action potential activity and synaptic transmission.

Original languageEnglish (US)
Pages (from-to)449-457
Number of pages9
JournalJournal of Neuroscience
Volume15
Issue number1 I
StatePublished - Jan 1995
Externally publishedYes

Fingerprint

Voltage-Gated Potassium Channels
Thyrotropin-Releasing Hormone
Neuropeptides
Gene Expression
Action Potentials
Neurotransmitter Agents
Messenger RNA
Endocrine Cells
Synaptic Transmission
Proteins
Down-Regulation
Genes

Keywords

  • gene expression
  • GH cells
  • membrane excitability
  • neuropeptide
  • pituitary
  • voltage-gated K channel

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Inhibition of voltage-gated K+ channel gene expression by the neuropeptide thyrotropin-releasing hormone. / Takimoto, Koichi; Gealy, Robert; Fomina, Alla F; Trimmer, James; Levitan, Edwin S.

In: Journal of Neuroscience, Vol. 15, No. 1 I, 01.1995, p. 449-457.

Research output: Contribution to journalArticle

Takimoto, Koichi ; Gealy, Robert ; Fomina, Alla F ; Trimmer, James ; Levitan, Edwin S. / Inhibition of voltage-gated K+ channel gene expression by the neuropeptide thyrotropin-releasing hormone. In: Journal of Neuroscience. 1995 ; Vol. 15, No. 1 I. pp. 449-457.
@article{f23afe39377d4953872ff373eeffda80,
title = "Inhibition of voltage-gated K+ channel gene expression by the neuropeptide thyrotropin-releasing hormone",
abstract = "Many neurotransmitters regulate action potential activity in neuronal, endocrine, and cardiac cells by rapidly modulating the gating of K+ channels. Neurotransmitters might also produce prolonged effects on excitability by regulating the expression of K+ channel genes. Here we show that the neuropeptide thyrotropin-releasing hormone (TRH) down-regulates Kv1.5 and Kv2.1 K+ channel mRNAs in clonal pituitary cells. The effect on Kv1.5 mRNA expression does not require protein synthesis and is due to decreased transcription. Immunoblots demonstrate that Kv1.5 and Kv2.1 immunoreactivities are significantly reduced by TRH within 12 hr. The change in channel protein expression is associated with a decrease in voltage-gated K+ currents. Thus, TRH enhances excitability by inhibiting K+ channel gene expression. Neuropeptide regulation of K+ channel gene expression may produce long-term changes in neuronal action potential activity and synaptic transmission.",
keywords = "gene expression, GH cells, membrane excitability, neuropeptide, pituitary, voltage-gated K channel",
author = "Koichi Takimoto and Robert Gealy and Fomina, {Alla F} and James Trimmer and Levitan, {Edwin S.}",
year = "1995",
month = "1",
language = "English (US)",
volume = "15",
pages = "449--457",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "1 I",

}

TY - JOUR

T1 - Inhibition of voltage-gated K+ channel gene expression by the neuropeptide thyrotropin-releasing hormone

AU - Takimoto, Koichi

AU - Gealy, Robert

AU - Fomina, Alla F

AU - Trimmer, James

AU - Levitan, Edwin S.

PY - 1995/1

Y1 - 1995/1

N2 - Many neurotransmitters regulate action potential activity in neuronal, endocrine, and cardiac cells by rapidly modulating the gating of K+ channels. Neurotransmitters might also produce prolonged effects on excitability by regulating the expression of K+ channel genes. Here we show that the neuropeptide thyrotropin-releasing hormone (TRH) down-regulates Kv1.5 and Kv2.1 K+ channel mRNAs in clonal pituitary cells. The effect on Kv1.5 mRNA expression does not require protein synthesis and is due to decreased transcription. Immunoblots demonstrate that Kv1.5 and Kv2.1 immunoreactivities are significantly reduced by TRH within 12 hr. The change in channel protein expression is associated with a decrease in voltage-gated K+ currents. Thus, TRH enhances excitability by inhibiting K+ channel gene expression. Neuropeptide regulation of K+ channel gene expression may produce long-term changes in neuronal action potential activity and synaptic transmission.

AB - Many neurotransmitters regulate action potential activity in neuronal, endocrine, and cardiac cells by rapidly modulating the gating of K+ channels. Neurotransmitters might also produce prolonged effects on excitability by regulating the expression of K+ channel genes. Here we show that the neuropeptide thyrotropin-releasing hormone (TRH) down-regulates Kv1.5 and Kv2.1 K+ channel mRNAs in clonal pituitary cells. The effect on Kv1.5 mRNA expression does not require protein synthesis and is due to decreased transcription. Immunoblots demonstrate that Kv1.5 and Kv2.1 immunoreactivities are significantly reduced by TRH within 12 hr. The change in channel protein expression is associated with a decrease in voltage-gated K+ currents. Thus, TRH enhances excitability by inhibiting K+ channel gene expression. Neuropeptide regulation of K+ channel gene expression may produce long-term changes in neuronal action potential activity and synaptic transmission.

KW - gene expression

KW - GH cells

KW - membrane excitability

KW - neuropeptide

KW - pituitary

KW - voltage-gated K channel

UR - http://www.scopus.com/inward/record.url?scp=0028802162&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028802162&partnerID=8YFLogxK

M3 - Article

VL - 15

SP - 449

EP - 457

JO - Journal of Neuroscience

JF - Journal of Neuroscience

SN - 0270-6474

IS - 1 I

ER -