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Lack of handling stress‐induced hyperthermia in orexin neuron‐ablated mice
Author(s) -
Kuwaki Tomoyuki,
Zhang Wei,
Sakurai Takeshi
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.788.18
Subject(s) - orexin , hyperthermia , endocrinology , medicine , orexin a , brown adipose tissue , chemistry , dynorphin , heart rate , knockout mouse , lateral hypothalamus , neuropeptide , blood pressure , hypothalamus , adipose tissue , opioid , receptor , opioid peptide
We have previously shown that multiple outputs during defense response against stressors (increases in blood pressure, heart rate, respiratory frequency and tidal volume, redistribution of blood flow from viscera to skeletal muscles, and stress‐induced analgesia) are attenuated in orexin‐deficient mice (Am J Physiol 290: R1654, 2006, Autonom Neurosci 142:11, 2008). In the present study, we examined whether the same is true for stress‐induced hyperthermia or not. We used prepro‐orexin knockout mice (ORX‐KO), orexin neuron‐ablated mice (ORX‐AB), and their controls. Increases in handling stress‐induced rectal temperature were significantly attenuated in ORX‐AB but not in ORX‐KO. Increases in uncoupling protein‐1, a major contributor in non‐shivering thermogenesis in the brown adipose tissue, were also blunted in ORX‐AB. Because orexinergic neurons contain not only orexin but also glutamate, dynorphin, and galanin, one of these substances should mediate stress‐induced hyperthermia.
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