Cold stress and corticotropin-releasing hormone induced changes in messenger ribonucleic acid for the α1-subunit of the L-type Ca2+ channel in the rat anterior pituitary and enriched populations of corticotropes

Jiangang Xie, Gregg Thomas Nagle, Aileen K. Ritchie, Thomas J. Collins, Gwen V. Childs

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

In response to stress, adrenocorticotropin (ACTH) is secreted from anterior pituitary corticotropes. Corticotropin-releasing hormone (CRH) is a potent stimulator of ACTH secretion. The CRH stimulation of secretion is mediated by cAMP and is largely dependent on Ca2+ influx through voltage-gated L-type Ca2+ channels. This study was designed to investigate whether the expression of L-type Ca2+ channels in the rat anterior pituitary and in corticotropes is regulated by acute stress and CRH, RNase protection assays were used to quantify α(1c) mRNA of the L-type Ca2+ channel. The α(1c) mRNA levels from stressed rats increased by 31% in anterior pituitaries of rats after 30 min of exposure to cold stress. Neither 60 min cold stress nor 30 min restraint stress had an effect on α(1c) mRNA levels. When α(1c) mRNA was detected by in situ hybridization in a population of corticotropes enriched to 90%, 0.5 nM CRH (3 h) stimulated a 36% increase in the average area of label/cell and a 10% increase in the average density of label. Our results suggest that (1) the expression of α(1c) subunit mRNA of L-type Ca2+ channels is increased in the rat anterior pituitary with a stress-specific response that might reflect an increase both in thyrotropes and corticotropes (both are known to be stimulated by cold stress), and (2) the CRH-mediated increase in α(1c) mRNA expression in individual rat corticotropes, in vitro, supports the hypothesis that some of the increase in vivo is due to changes in corticotropes.

Original languageEnglish (US)
Pages (from-to)10-19
Number of pages10
JournalNeuroendocrinology
Volume70
Issue number1
DOIs
StatePublished - Jul 24 1999

Fingerprint

Corticotropin-Releasing Hormone
RNA
Messenger RNA
Adrenocorticotropic Hormone
Population
Ribonucleases
In Situ Hybridization

Keywords

  • Ca channels
  • Corticotropes
  • Corticotropin
  • Corticotropin-releasing hormone
  • Immunocytochemistry
  • In situ hybridization
  • Molecular neuroendocrinology
  • Stress

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

Cite this

Cold stress and corticotropin-releasing hormone induced changes in messenger ribonucleic acid for the α1-subunit of the L-type Ca2+ channel in the rat anterior pituitary and enriched populations of corticotropes. / Xie, Jiangang; Nagle, Gregg Thomas; Ritchie, Aileen K.; Collins, Thomas J.; Childs, Gwen V.

In: Neuroendocrinology, Vol. 70, No. 1, 24.07.1999, p. 10-19.

Research output: Contribution to journalArticle

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title = "Cold stress and corticotropin-releasing hormone induced changes in messenger ribonucleic acid for the α1-subunit of the L-type Ca2+ channel in the rat anterior pituitary and enriched populations of corticotropes",
abstract = "In response to stress, adrenocorticotropin (ACTH) is secreted from anterior pituitary corticotropes. Corticotropin-releasing hormone (CRH) is a potent stimulator of ACTH secretion. The CRH stimulation of secretion is mediated by cAMP and is largely dependent on Ca2+ influx through voltage-gated L-type Ca2+ channels. This study was designed to investigate whether the expression of L-type Ca2+ channels in the rat anterior pituitary and in corticotropes is regulated by acute stress and CRH, RNase protection assays were used to quantify α(1c) mRNA of the L-type Ca2+ channel. The α(1c) mRNA levels from stressed rats increased by 31{\%} in anterior pituitaries of rats after 30 min of exposure to cold stress. Neither 60 min cold stress nor 30 min restraint stress had an effect on α(1c) mRNA levels. When α(1c) mRNA was detected by in situ hybridization in a population of corticotropes enriched to 90{\%}, 0.5 nM CRH (3 h) stimulated a 36{\%} increase in the average area of label/cell and a 10{\%} increase in the average density of label. Our results suggest that (1) the expression of α(1c) subunit mRNA of L-type Ca2+ channels is increased in the rat anterior pituitary with a stress-specific response that might reflect an increase both in thyrotropes and corticotropes (both are known to be stimulated by cold stress), and (2) the CRH-mediated increase in α(1c) mRNA expression in individual rat corticotropes, in vitro, supports the hypothesis that some of the increase in vivo is due to changes in corticotropes.",
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AU - Nagle, Gregg Thomas

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AU - Childs, Gwen V.

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