Rapid Changes in Somatostatin and TRH mRNA in Whole Rat Hypothalamus in Response to Acute Cold Exposure
作者:
Florence Rage,
Jean‐Bernard Lazaro,
Ahmed Benyassi,
Sandor Arancibia,
Lucia Tapia‐Arancibia,
期刊:
Journal of Neuroendocrinology
(WILEY Available online 1994)
卷期:
Volume 6,
issue 1
页码: 19-23
ISSN:0953-8194
年代: 1994
DOI:10.1111/j.1365-2826.1994.tb00550.x
出版商: Blackwell Publishing Ltd
关键词: cold exposure;somatostatin;TRH;mRNA;hypothalamus
数据来源: WILEY
摘要:
AbstractAcute cold stimulus induces activation of the thyreotropic axis characterized by a rapid increase in plasma thyrotropin (TSH). Since pituitary TSH release is mainly regulated by two hypothalamic hormones: thyrotropin‐releasing hormone (TRH) and somatostatin, the aim of this study was to analyse whether changes in the steady state mRNA levels and peptide content of these neurohormones occur under acute cold stimulation in rats. Northern blot analysis of hypothalamic somatostatin mRNA levels after 15, 30, 60 or 180 min of cold exposure revealed a 2.0‐fold increase after 15 min at 4°C. This augmentation was followed by a return to control values at 30 min. However, the hypothalamic content of somatostatin was not significantly modified at any cold exposure time. TRH mRNA showed a similar pattern to somatostatin, with a 2.5‐fold increase after 15 min at 4°C. In contrast, hypothalamic TRH content was significantly decreased after 15 min cold exposure, returning to control values at 30 min. The increase in mRNA levels was specific for the two hypothalamic hormones, since there was no concomitant variation in GAPDH mRNA used as negative control. These results suggest that the organism is quickly aroused by cold stimulus, triggering rapid activation in transcription of the two neurohormones involved in the regulation of the thyreotrope axis. Since the peptide contents did not show the same pattern, a quantitative change in transcription or in mRNA stability does not appear to be a prerequisite for increased peptide expression, suggesting that somatostatin and TRH gene expressions could be regulated at translational or post‐translatio
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