Open AccessUrocortin-Deficient Mice Display Normal Stress-Induced Anxiety Behavior and Autonomic Control but an Impaired Acoustic Startle Response
Author(s) -
Xiaozhong Wang,
Hua Su,
Leslie D. Copenhagen,
Sukishi Vaishnav,
Fredalina Pieri,
Cynthia Shope,
William E. Brownell,
Mariella De Biasi,
Richard Paylor,
Allan Bradley
Publication year - 2002
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.22.18.6605-6610.2002
Subject(s) - urocortin , startle response , neuropeptide , biology , neuroscience , endocrinology , startle reaction , medicine , autonomic nervous system , corticotropin releasing hormone , reflex , receptor , hormone , heart rate , blood pressure
Corticotropin-releasing hormone (Crh) plays an important role in modulating physiological and behavioral responses to stress. Its actions are mediated through two receptors, Crhr1 and Crhr2. Urocortin (Ucn), a Crh-related neuropeptide and the postulated endogenous ligand for Crhr2, is a potential mediator of stress responses. We generated Ucn-deficient mice using embryonic stem cell technology to determine its role in stress-induced behavioral and autonomic responses. Unlike Crhr1- or Crhr2-deficient mice, Ucn-deficient mice exhibit normal anxiety-like behavior as well as autonomic regulation in response to stress. However, the mutant mice display an impaired acoustic startle response that is not due to an obvious hearing defect. Thus, our results suggest that Ucn does not play an essential role in stress-induced behavioral and autonomic responses. Ucn may modulate the acoustic startle response through the Ucn-expressing neuron projections from the region of the Edinger-Westphal nucleus.