Chapter title |
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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Chapter number | 26 |
Book title |
Arterial Chemoreception
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Published in |
Advances in experimental medicine and biology, January 2012
|
DOI | 10.1007/978-94-007-4584-1_26 |
Pubmed ID | |
Book ISBNs |
978-9-40-074583-4, 978-9-40-074584-1
|
Authors |
Reyes, Edison-Pablo, Abarzúa, Sebastián, Martin, Aldo, Rodríguez, Jorge, Cortés, Paula P, Fernández, Ricardo, Edison-Pablo Reyes, Sebastián Abarzúa, Aldo Martin, Jorge Rodríguez, Paula P. Cortés, Ricardo Fernández, Cortés, Paula P. |
Abstract |
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. |
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