Possible Interaction: Capsaicin and Cholecystokinin

“Because it has been reported that systemic or perivagal capsaicin pretreatment abolishes the effects of CCK , the aim of the present work was to investigate the response of cNTS neurons to CCK-8s in vagally deafferented rats.”

“ Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK.”

“When CCK was administered during gastric distension, it significantly enhanced NTS Fos expression in response to distension in Cap rats.”

“These results suggest that capsaicin influence neuropeptides such as orexigenic NPY and anorexigenic CCK related to control food intake.”

“It was expected that only capsaicin-sensitive C-type neurons would respond to CCK, because most vagally mediated actions of CCK are blocked by capsaicin treatment.”

“Perivagal application of capsaicin increased plasma CCK levels and significantly increased pancreatic wet weight compared with those in the control rats.”

“The pretreatment with L-NNA to inhibit NO-synthase activity attenuated significantly the protective and hyperemic effects of CCK but not those of leptin while capsaicin denervation counteracted leptin-induced protection and rise in the GBF but attenuated significantly those of CCK.”

“In conscious rats, perivagal application of capsaicin abolished the pancreatic response evoked by physiological doses of CCK and intraduodenal administration of maltose or hypertonic saline, confirming the physiological relevance of the observations in anaesthetized rats.”

“The hyperemia, but not the protection, afforded by CCK and pentagastrin was reduced after sensory nerve deactivation with capsaicin.”

“Treatment of neonatal rats with capsaicin attenuated the satiety effect of injected CCK in adult life.”

“ Capsaicin treatment attenuates suppression of food intake induced by systemic administration of cholecystokinin (CCK) but not by gastric distension.”