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Functional neuroanatomy of the parvocellular vasopressinergic system: transcriptional responses to stress and glucocorticoid feedback.

Authors
Type
Published Article
Journal
Progress in brain research
0079-6123
Publication Date
Volume
119
Pages
31–43
Identifiers
PMID: 10074779
Source
Medline
License
Unknown

Abstract

This chapter summarizes the regulation of vasopressin (VP) transcription within the parvocellular neurosecretory cells of the hypothalamic paraventricular nucleus in vivo, with special reference to stress-response and glucocorticoid feedback. VP is commonly held as the first and the most potent among the co-secretagogues that act synergistically with corticotropin-releasing factor (CRF-41) to induce adrenocorticotropin (ACTH) from the anterior pituitary in response to various internal and external stimuli. Cellular levels of the primary transcripts of VP and CRF genes, revealed by in situ hybridization histochemistry using probes complementary to intronic sequences, are increased after acute challenges with different time courses. In contrast to the rapid stress-induced upregulation of CRF gene expression, VP transcription shows a delayed increase suggesting different regulatory mechanisms governing the two main ACTH releasing neuropeptides in the parvocellular neurosecretory neurons. With respect of transcription factors that may mediate these effects, besides rapid phosphorylation of the cAMP-response element-binding protein (CREB), VP activation in the parvocellular neurons requires additional newly synthesized factors such as those encoded by immediate-early genes, like c-fos. In addition, it has recently been revealed that glucocorticoid negative feedback during stress, selectively targets vasopressin transcription in the parvocellular neurons that is likely mediated by interaction of glucocorticoid receptors and immediate-early gene products. These data speak for the emerging consensus that VP is the principal factor that imparts situation-specific drive and represents the regulated variable governing hypothalamo-pituitary-adrenocortical axis during stress.

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