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Recurrent hypoglycemia alters hypothalamic expression of the regulatory proteins FosB and synaptophysin

Show simple item record Al-Noori, Salwa Sanders, Nicole M. Taborsky, Gerald J. Wilkinson, Charles W. Zavosh, Aryana West, Connie Sanders, Colleen M. Figlewicz, Dianne P. 2011-11-07T21:21:41Z 2011-11-07T21:21:41Z 2008-08-27
dc.identifier.citation Am J Physiol Regul Integr Comp Physiol. 2008 November; 295(5): R1446–R1454. en_US
dc.description.abstract A limiting factor to the clinical management of diabetes is iatrogenic hypoglycemia. With multiple hypoglycemic episodes, the collective neuroendocrine response that restores euglycemia is impaired. In our animal model of recurrent hypoglycemia (RH), neuroendocrine deficits are accompanied by a decrease in medial hypothalamic activation. Here we tested the hypothesis that the medial hypothalamus may exhibit unique changes in the expression of regulatory proteins in response to RH. We report that expression of the immediate early gene FosB is increased in medial hypothalamic nuclei, anterior hypothalamus, and posterior paraventricular nucleus of the thalamus (THPVN) of the thalamus following RH. We identified the hypothalamic PVN, a key autonomic output site, among the regions expressing FosB. To identify the subtype(s) of neuronal populations that express FosB, we screened candidate neuropeptides of the PVN for coexpression using dual fluorescence immunohistochemistry. Among the neuropeptides analyzed [including oxytocin, vasopressin, thyrotropin-releasing hormone, and corticotropinreleasing factor (CRF)], FosB was only identified in CRF-positive neurons. Inhibitory !-aminobutyric acid-positive processes appear to impinge on these FosB-expressing neurons. Finally, we observed a significant decrease in the presynaptic marker synaptophysin within the PVN of RH-treated vs. saline-treated rats, suggesting that rapid alterations of synaptic morphology may occur in association with RH. Collectively, these data suggest that RH stress triggers cellular changes that support synaptic plasticity, in specific neuroanatomical sites, which may contribute to the development of hypoglycemia-associated autonomic failure. Keywords: FosB, recurrent hypoglycemia, paraventricular nucleus, corticotropin- en_US
dc.publisher American Journal of Physiology en_US
dc.subject FosB, recurrent hypoglycemia, paraventricular nucleus, corticotropin-releasing factor, synaptophysin en_US
dc.title Recurrent hypoglycemia alters hypothalamic expression of the regulatory proteins FosB and synaptophysin en_US
dc.type Article en_US

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