Impaired stress response and reduced anxiety in mice lacking a functional corticotropin-releasing hormone receptor 1

@article{Timpl1998ImpairedSR,
  title={Impaired stress response and reduced anxiety in mice lacking a functional corticotropin-releasing hormone receptor 1},
  author={Peter Timpl and Rainer Spanagel and Inge Sillaber and Adelheid E Kresse and Johannes M. H. M. Reul and G{\"u}nter Stalla and V{\'e}ronique Blanquet and Thomas Steckler and Florian Holsboer and Wolfgang Wurst},
  journal={Nature Genetics},
  year={1998},
  volume={19},
  pages={162-166}
}
Corticotropin-releasing hormone (CRH) is a potent mediator of endocrine, autonomic, behavioural and immune responses to stress, and has been implicated in the stress-like and other aversive consequences of drug abuse, such as withdrawal from alcohol. Two CRH receptors, Crhr1 and Crhr2, have been identified in the mouse. Crhr1 is highly expressed in the anterior pituitary, neocortex, hippocampus, amygdala and cerebellum, and activation of this receptor stimulates adenylate cyclase. Here we show… 

Abnormal adaptations to stress and impaired cardiovascular function in mice lacking corticotropin-releasing hormone receptor-2

It is shown that Crhr2 supplies regulatory features to the hypothalamic-pituitary-adrenal axis (HPA) stress response and is essential for sustained feeding suppression induced by Ucn, and specific responses in the brain and periphery that involve Cr hr2 are identified.

Altered anxiety and weight gain in corticotropin-releasing hormone-binding protein-deficient mice.

An important role for CRH-BP is suggested in maintaining appropriate levels of these peptides in the central nervous system in maintainingappropriate levels of CRH and/or urocortin levels in the brain of CRh-BP-deficient animals.

Limbic corticotropin-releasing hormone receptor 1 mediates anxiety-related behavior and hormonal adaptation to stress

The data clearly show that limbic Crhr1 modulates anxiety-related behavior and that this effect is independent of HPA system function, and provide evidence for a new role of limbicCrhr1 in neuroendocrine adaptation to stress.

Conditional mouse mutants highlight mechanisms of corticotropin-releasing hormone effects on stress-coping behavior

Enhanced noradrenergic activity was identified as potential molecular mechanism underlying increased active stress-coping behavior observed in these animals and may serve as animal models for stress-elicited pathologies and treatments that target the central CRH system.

Stress-induced behaviors require the corticotropin-releasing hormone (CRH) receptor, but not CRH.

An unidentified CRH-like molecule other than CRH or urocortin, acting through the CRH receptors in brain regions believed to mediate stress-induced behaviors, may mediate the behavioral response to stress, either alone or in concert with CRH.

Mice deficient for corticotropin-releasing hormone receptor-2 display anxiety-like behaviour and are hypersensitive to stress

Corticotropin-releasing hormone (Crh) is a critical coordinator of the hypothalamic-pituitary-adrenal (HPA) axis and Crhr2-mutant mice are hypersensitive to stress and display increased anxiety-like behaviour.

Corticotrophin Releasing Factor-Induced Synaptic Plasticity in the Amygdala Translates Stress into Emotional Disorders

Results show for the first time a stress peptide-induced behavioral syndrome that can be correlated with cellular mechanisms of neural plasticity, a novel mechanism that may explain the etiological role of stress in several chronic psychiatric and medical disorders.

Inhibition of corticotropin releasing factor expression in the central nucleus of the amygdala attenuates stress-induced behavioral and endocrine responses

It appears that while CRF projecting from the CeA does not play a significant role in the expression stress-induced anxiety-like behaviors on the EPM and OF it does play a critical role in stress- induced HPA activation.

Loss of hypothalamic corticotropin-releasing hormone markedly reduces anxiety behaviors in mice

It is reported that hypothalamus-specific Crh knockout mice (Sim1CrhKO mice) have absent Crh mRNA and peptide mainly in the paraventricular nucleus of the hypothalamus but preserved Crh expression in other brain regions including amygdala and cerebral cortex, consistent with the existence of PVHCrh-dependent behavioral pathways.
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