Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic injections of cholecystokinin octapeptide sulfate ester (CCK-8-SE) elicit various behavioral and autonomic responses, such as increases in nonrapid-eye-movement sleep (NREMS) and hypothermia. There are two CCK receptors; both CCK-A and CCK-B receptors are stimulated by CCK-8-SE. The relative importance of the CCK-A and CCK-B receptors in the somnogenic and hypothermic effects of CCK-8-SE is not well understood. In the present experiments, we studied the effects of the selective activation of CCK-B receptors by CCK tetrapeptide (CCK-4) or nonsulfated CCK-8 (CCK-8-NS) on sleep and brain temperature (Tbr). Rats were injected intraperitoneally with saline on the control day and with CCK-8-NS (10, 50, or 250 microg/kg) or CCK-4 (10, 50, or 250 microg/kg) on the test day 5-10 min before dark onset. Electroencephalogram, electromyogram, and Tbr were recorded for 12 h. None of the treatments affected sleep or Tbr significantly, with the exception of 10 microg/kg CCK-4, which transiently decreased the amount of NREMS, and 10 microg/kg CCK-8-NS, which slightly increased REMS. These results suggest that the activation of CCK-B receptors by systemic injection of CCK-4 or CCK-8-NS is not sufficient to elicit increased NREMS and hypothermia in rats.
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PMID:Selective activation of CCK-B receptors does not induce sleep and does not affect EEG slow-wave activity and brain temperature in rats. 922 59

Thermoregulatory effects of cholecystokinin (CCK) peptides are reviewed with special emphasis on two types of responses, that is hyperthermia (fever) and hypothermia. Central microinjection of CCK in rats induces a thermogenic response that can be attenuated by CCK-B receptor antagonists, but some authors observed a hypothermia. By contrast to its central fever-inducing effect, in rodents exposed to cold CCK-8 elicits a dose-dependent hypothermia on peripheral injection probably acting on CCK-A receptors. It is suggested that neuronal CCK may have a specific role in the development of hyperthermia, and endogenous CCK-ergic mechanisms could contribute to the mediation of fever. The possible role of CCK-ergic mediation in endotoxin (LPS) fever has revealed that while CCK-B receptors seem to be involved in the development of fever, the role of CCK-A receptors could be more complex. In particular, while rats lacking functional CCK-A receptors show an exaggerated fever response, this phenomenon may be associated with a trait different from the absence of this receptor set. The relationship between the putative CCK-ergic febrile mechanism and the established central PGE mediation needs further study.
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PMID:Cholecystokinin: possible mediator of fever and hypothermia. 1476 68