Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2005) 9 P230

BES2005 Poster Presentations Clinical (51 abstracts)

Differential regulation of Urocortin 3 mRNA expression in the central nervous system by stress and glucocorticoids

PM Jamieson , C Li , J Vaughan & W Vale


Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, La Jolla, USA.


The CRF-related ligand Urocortin 3 (Ucn 3) is expressed in discrete subcortical areas with highest mRNA levels in the medial amgydala (MEA), hypothalamic median preoptic nucleus (MePO) and the rostral part of the perifornical hypothalamic area (PFN). Close anatomical association between major Ucn 3 terminal fields and the type 2-CRF receptor in hypothalamus, lateral septum and medial amygdala suggest it is well placed to modulate physiological processes including behavioural, hormonal and metabolic responses to stress. Male rats were subjected to various stressors and Ucn 3 mRNA in MEA, PFN and MePO quantified by in situ hybridization. Chronic caloric restriction or excess (60percent control consumption or high fat diet for 8 weeks) did not alter expression. 48hr food deprivation did not alter expression in PFN and MePO but significantly decreased levels in the MEA. Likewise, haemorrhagic stress (25percent blood volume removed) decreased expression in the MePO after 30min. 30min following onset of restraint stress, Ucn 3 expression was increased in the MEA with a trend to increased expression in PFN and MePO. Following both restraint and haemorrhage, levels had returned to baseline by 4hrs. 10 days after adrenalectomy (ADX), Ucn 3 expression in the PFN was increased. Corticosterone (B) replacement to ADX rats restored levels to those of sham-operated controls. ADX or ADXplusB did not alter expression in MEA or MePO. These results do not support a role for Ucn 3 in control of long term maintenance of energy homeostasis. However, rapid changes in expression in the MEA following stressors is consistent with a role for Ucn 3 in modulating acute stress responses. Differential regulation in MEA and PFA by stressors and ADX suggests glucocorticoids are not responsible for Ucn 3 responses to acute stressors, but may be a physiological regulator under other circumstances with potential consequences for the HPA axis. All experimental protocols and procedures were approved by The Salk Institute Animal Use and Care Committee.

Volume 9

24th Joint Meeting of the British Endocrine Societies

British Endocrine Societies 

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