@article{00b8b292a2ab4ae396db6561f9ecf8a5,
title = "Tectal corticotropin-releasing factor (CRF) neurons respond to fasting and a reactive stressor in the African Clawed Frog, Xenopus laevis",
abstract = "It is well established that hypothalamic neurons producing the peptide corticotropin-releasing factor (CRF) play a key role in stress adaptation, including reduction of food intake when a threat or stressor is present. We have previously reported on the presence of an intrinsic CRF signaling system within the optic tectum (OT), a brain area that plays a key role in visually guided prey capture/predator avoidance decisions. To better understand the potential role of tectal CRF neurons in regulating adaptive behavior and energy balance during stress we examined evidence for modulation of tectal CRF neuronal activity after stressor exposure and food deprivation in the African clawed frog Xenopus laevis. We tested two predictions, 1) that exposure to categorically distinct stressors (ether vapors and shaking) will reduce food intake and modulate the activity of tectal CRF cells, and 2) that food deprivation will modulate the activity of tectal CRF cells. Exposure to ether increased tectal content of CRF and CRF transcript, but lowed CRFR1 transcript abundance. Two weeks of food deprivation reduced total fat stores in frogs and decreased tectal content of CRF content while having no effect on CRF and CRFR1 transcript abundance. Our data are consistent with a role for tectal CRF neurons in modulating food intake in response to certain stressors.",
keywords = "Amphibian, Anxiety, Fear, Foraging, Stress, Vision",
author = "Christine Prater and Carlos Garcia and Liam McGuire and James Carr",
note = "Funding Information: This paper was presented in part in a symposium at the 28th Conference of European Comparative Endocrinologists in Leuven, Belgium, August 21–25, 2016. We thank Gudrun De Boeck (Antwerp, Belgium) and Patrick Kestemont (Namur, Belgium) for organizing the symposium. We thank Dr. R. Denver (U. Michigan) for supplying xCRF antiserum and xCRF peptide. This work was supported by funding from the Texas Tech Department of Biological Sciences, Texas Tech University Association of Biologists (TTUAB) , Texas Tech Obesity Research Cluster (ORC) , Texas Tech University Graduate School , and the National Sciences Foundation IOS # 1656734 . Funding Information: This paper was presented in part in a symposium at the 28th Conference of European Comparative Endocrinologists in Leuven, Belgium, August 21–25, 2016. We thank Gudrun De Boeck (Antwerp, Belgium) and Patrick Kestemont (Namur, Belgium) for organizing the symposium. We thank Dr. R. Denver (U. Michigan) for supplying xCRF antiserum and xCRF peptide. This work was supported by funding from the Texas Tech Department of Biological Sciences, Texas Tech University Association of Biologists (TTUAB), Texas Tech Obesity Research Cluster (ORC), Texas Tech University Graduate School, and the National Sciences Foundation IOS #1656734. Publisher Copyright: {\textcopyright} 2017",
year = "2018",
month = mar,
day = "1",
doi = "10.1016/j.ygcen.2017.07.029",
language = "English",
volume = "258",
pages = "91 -- 98",
journal = "General and Comparative Endocrinology",
publisher = "Elsevier",
}