LPS-Induced c-Fos Activation in NTS Neurons and Plasmatic Cortisol Increases in Septic Rats Are Suppressed by Bilateral Carotid Chemodenervation
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Lipopolysaccharide (LPS) administered i.p. increases significantly the activation of c-Fos in neurons of the nucleus of the solitary tract (NTS), which in turn activates hypothalamus-pituitary-adrenal axis. The vagus nerve appears to play a role in conveying cytokines signals to the central nervous system (CNS), since -in rodent models of sepsis- bilateral vagotomy abolishes increases in plasmatic glucocorticoid levels, but does not suppress c-Fos NTS activation. Considering that NTS also receives sensory inputs from carotid body chemoreceptors, we evaluated c-Fos activation and plasmatic cortisol levels 90 min after i.p. administration of 15 mg/kg LPS. Experiments were performed in male Sprague–Dawley rats, in control conditions and after bilateral carotid neurotomy (BCN). LPS administration significantly increases the number of c-Fos positive NTS neurons and plasmatic cortisol levels in animals with intact carotid/sinus nerves. When LPS was injected after BCN, the number of c-Fos positive NTS neurons, and plasmatic cortisol levels were not significantly modified. Our data suggest that carotid body chemoreceptors might mediate CNS activation during sepsis.
KeywordsLPS Inflammation Carotid sinus nerve c-Fos NTS
Special thanks are due to Mrs. Carolina Larraín for proofreading the manuscript. This work was supported by grant DI-40-11/R (to RF), from the Division for Research of the Universidad Andres Bello (UNAB).
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