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Ootsuka, Y., Blessing, W.W., Steiner, A.A. and Romanovsky, A.A. (2008) Fever response to intravenous prostaglandin E2 is mediated by the brain but does not require afferent vagal signaling. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 294, R1294-R1303. doi:10.1152/ajpregu.00709.2007

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• TITLE: Body temperature control in fever modeling after preliminary injection of glutamate receptors ligands into the solitary tract nucleus

  AUTHORS: Stanislav V. Koulchitsky, Svetlana G. Pashkevich, Nastassia M. Navasiolava, Marc-Antoine Custaud, Vladimir A. Kulchitsky

  KEYWORDS: Escherichia coli; Endotoxin; Brainstem; Fever; Control Body Temperature; Defense Reflexes

  JOURNAL NAME: Advances in Bioscience and Biotechnology, Vol.4 No.4, April 19, 2013

  ABSTRACT: Deep body temperature of 57 male Wistar rats was measured in response to systemic (i.v. or i.p.) injection of Escherichia coli lipopolysaccharide (LPS). Animals were preliminarily (4 weeks before the experiment) treated with microinjections of the toxic dose of glutamate receptors agonists or vehicle into solitary tract nucleus or caudal part of ventrolateral medulla. Microinjections of the glutamate receptors agonists provoked a local destruction of brain tissue, which was accompanied by the significant transformation (amplification or attenuation) of temperature response to the systemic injection of 3 μg/kg E. coli LPS. Animals treated with vehicle did not demonstrate significant changes in their response to LPS. Obtained data testify that impairment of central nervous structure involved in the regulation and maintenance of deep body temperature is accompanied by atypical development of E. coli LPS-induced fever.