Abstract
We examined core body temperature (CBT) of urocortin 1 (UCN1) and corticotropin releasing factor (CRF) knockout (KO) mice exposed to 4°C for 2 h. UCN1KO mice showed higher average CBT during cold exposure as compared to WT. The CBT of male and female WT mice dropped significantly to34.1 ± 2.4and34.9 ± 3.1 C at 4°C, respectively. In contrast, the CBT of male and female UCN1KO mice dropped only slightly after 2 h at 4°C to36.8 ± 0.7and38.1 ± 0.5 C, respectively. WT female and male UCN1KO mice showed significant acclimatization to cold; however, female UCN1KO mice did not show such a significant acclimatization. CRFKO mice showed a dramatic decline in CBT from38.2 ± 0.4at 22°C to26.1 ± 9.8at 4°C for 2 h. The CRF/UCN1 double KO (dKO) mice dropped their CBT to32.5 ± 4.0after 2 h exposure to 4°C. Dexamethasone treatment prevented the decline in CBT of the CRFKO and the dKO mice. Taken together, the data suggest a novel role for UCN1 in thermoregulation. The role of CRF is likely secondary to adrenal glucocorticoids, which have an important regulatory role on carbohydrate, fat, and protein metabolism.
Highlights
Corticotropin releasing factor (CRF) [1] plays an essential role in the physiological regulation of the hypothalamicpituitary-adrenal (HPA) as CRF knockout (KO) mice have low concentrations of corticosterone and decreased response to stress [2]
CRF is found in several regions of the central nervous system (CNS) where it functions as a neurotransmitter and regulates several aspects of behavior in response to stressful stimuli [3]
We compared the averages of all values taken during the 120 min at 4∘C between WT and UCN1KO mice (Table 1)
Summary
Corticotropin releasing factor (CRF) [1] plays an essential role in the physiological regulation of the hypothalamicpituitary-adrenal (HPA) as CRF knockout (KO) mice have low concentrations of corticosterone and decreased response to stress [2]. The urocortins, UCN1 [4], UCN2 [5], and UCN3 [6], are a family of peptides, which were discovered by their sequence homology to CRF, sauvagine [7], and urotensin 1 [8]. These peptides bind and activate the CRF receptors, CRFR1 [9] and CRFR2 [10], with different affinities and potencies. UCN1-deficient mice were shown to have a normal corticosterone response to acute immobilization stress [13, 14]; they showed anxiety-like behavior and impaired inner ear physiology [13]. We assessed the hypothesis that UCN1 may be important for the maintenance of core body temperature during exposure to cold environment and examined the acclimatization of the core body temperature to a 2 h cold exposure of mice deficient in UCN1, CRF, or both
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