Several effects of bacterial
endotoxins involve an
opioid pathway and
neuropeptide FF is an endogenous
peptide known to modulate
opioid activity, mainly in the central nervous system. The aim of this study was to investigate in rats the role of central
neuropeptide FF receptors in intestinal motor disturbances and
body temperature changes induced by
endotoxins and
platelet-activating factor (PAF), a major
endotoxin mediator. Rats were fitted with intestinal
electrodes, an intraperitoneal thermistor probe and an intracerebroventricular (i.c.v.)
cannula for long-term use. E. coli
endotoxin (100 microg/kg, i.v.) disrupted the cyclic pattern of intestinal migrating myoelectric complexes and induced a biphasic increase in body temperature while PAF (25 microg/kg, i.p.) disrupted the migrating myoelectric complexes and
induced hypothermia for about 2 h. The
neuropeptide FF analog, (1 DME)Y8Fa (D-Tyr-D-Leu[N-Me]-Phe-Gln-Pro-Gln-Arg-Phe-NH2) administered i.c.v. 40 and 100 microg/kg reduced the duration of migrating myoelectric complex disruption induced by
endotoxin and PAF and abolished the PAF-
induced hypothermia. Only at the dose of 100 microg/kg did (1 DME)Y8Fa change the biphasic
endotoxin-
induced hyperthermia into a monophasic increase.
Naloxone (1 mg/kg, s.c.) reduced only the duration of migrating myoelectric complex disruption induced by
endotoxin. These results indicate that central
neuropeptide FF modulates the intestinal motor disturbances and changes in body temperature induced by
endotoxin and PAF. Its action against
endotoxin may involve an anti-
opioid pathway whereas its action against PAF does not.