It is well known that endo
cannabinoids play an important role in the regulation of food intake and body weight. Endo
cannabinoids and
cannabinoid re
ceptors are found in the hypothalamus and brainstem, whi
ch are
central areas involved in the
control of food intake and energy expenditure. A
ctivation of these areas is related to hypophagia observed during inflammatory stimulus. This study investigated the effe
cts of
cannabinoid (CB
1) re
ceptor blo
ckade on lipopolysa
ccharide (LPS)-indu
ced hypophagia. Male Wistar rats were pretreated with rimonabant (10聽mg/kg, by gavage) or vehi
cle; 30聽min later they re
ceived an inje
ction of either LPS (100聽渭g/kg, intraperitoneal) or saline. Food intake, body weight,
corti
costerone response, CRF and CART mRNA expression, Fos-CRF and Fos-伪-MSH immunorea
ctivity in the hypothalamus and Fos-tyrosine hydroxylase (TH) immunorea
ctivity in the brainstem were evaluated. LPS administration de
creased food intake and body weight gain and in
creased plasma
corti
costerone levels and CRF mRNA expression in the PVN. We also observed an in
crease in Fos-CRF and Fos-TH double-labeled neurons after LPS inje
ction in vehi
cle-pretreated rats, with no
changes in CART mRNA or Fos-伪-MSH immunorea
ctive neurons in the ARC. In saline-treated animals, rimonabant pretreatment de
creased food intake and body weight gain but did not modify hormone response or Fos expression in the hypothalamus and brainstem
compared with vehi
cle-pretreated rats. Rimonabant pretreatment potentiated LPS-indu
ced hypophagia, body weight loss and Fos-CRF and Fos-TH expressing neurons. Rimonabant did not modify
corti
costerone, CRF mRNA or Fos-伪-MSH responses in rats treated with LPS. These data suggest that the endo
cannabinoid system, mediated by CB
1 re
ceptors, modulates hypothalami
c and brainstem
cir
cuitry underlying the hypophagi
c effe
ct during endotoxemia to prevent an exaggerated food intake de
crease.
This article is part of a Special Issue entitled 鈥楥entral Control of Food Intake鈥?