LPS-induced c-Fos activation in NTS neurons and plasmatic cortisol increases in septic rats are suppressed by bilateral carotid chemodenervation.
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.
Clínica Alemana-Universidad del Desarrollo, Lo Barrenechea, Santiago, Chile.
Edison-Pablo
EP
Reyes
Sebastián
S
Abarzúa
Aldo
A
Martin
Jorge
J
Rodríguez
Paula P
PP
Cortés
Ricardo
R
Fernández
D000818:Animals; D002344:Carotid Body / Q000502:physiology*; D006854:Hydrocortisone / Q000097:blood*; D008297:Male; D009407:Nerve Block; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000097:blood*; D017552:Solitary Nucleus / Q000378:metabolism*; D014630:Vagus Nerve / Q000502:physiology
D016760:Proto-Oncogene Proteins c-fos; D006854:Hydrocortisone