Abstract
Using in situ hybridization histochemistry, corticotropin-releasing hormone gene expression is first detectable in the parvocellular portion of the rat paraventricular nucleus on the 17th fetal day. The prevalence of messenger RNA for corticotropin releasing hormone decreases perinatally, specifically between the 19th and 21st fetal days. By the 4th postnatal day, CRH gene expression is similar to that of the adult rat. Somatostatin messenger-RNA is detectable on the 14th fetal day in the periventricular nucleus. No perinatal hiatus in somatostatin gene expression is evident.
Highlights
Corticotropin releasing hormone (CRH), synthesized in the hypothalamic paraventricular nucleus (PVN), mediates the release of adrenocorticotropic hormone (ACTH) and corticosteroids in response to stressful stimuli, as part of the brain-pituitary-adrenal axis.‘* During the perinatal period in the rat, i.e. the stress non-responsive period, little perturbation of hormonal levels occurs in response to noxious events.’ The relationship between the regulation of CRH gene expression during late fetal and perinatal periods, and the onset of the stress-non-responsive-period has not been elucidated
Optical density was determined over the paraventricular nucleus, as well as over the parietal cortex for CRH-mRNA assessment; optical density (OD) over the latter was defined as background
In this study, using adjacent sections of the same brains, we investigated the ontogeny of CRH and somatostatin gene expression in the rat diencephalon
Summary
Title Ontogeny of corticotropin releasing hormone gene expression in rat hypothalamus--comparison with somatostatin. Journal International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 9(5)
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