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CRH-R2, as noted above, binds the urocortins 1, 2 and 3, and appears to mediate a down-regulatory role in the HPA response to stress: knockout mice exhibit a hypersensitive acute ACTH and corticosterone response (198) and a defective recovery from stress with a slower drop in corticosterone (199)

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The increase in reactive oxygen species (ROS) and inadequate antioxidant defences render the brain vulnerable to oxidative damage, leading to the development of many inflammatory and degenerative neurological diseases [75, 76]