The central role of corticotropin-releasing hormone in stress-induced hyperthermia and LPS-induced fever in rats
- VernacularTitle:中枢CRH在大鼠应激性体温升高和LPS性发热机制中的作用
- Author:
Huadong WANG
;
Yang QU
;
Yanping WANG
;
Yuxia YAN
;
Yongmei FU
;
Daxiang LU
;
Chuji LI
- Publication Type:Journal Article
- Keywords:
Corticotropin releasing hormone;
Arginine vasopressin;
Lipopolysaccharide;
Fever;
Body temperature regulation
- From:
Chinese Journal of Pathophysiology
1986;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To further investigate the role of central corticotropin-releasing hormone in stress-induced hyperthermia and lipopolysaccharide (LPS)-induced fever in the rat. METHODS: Test substances were administered intracerebroventricularly (icv) via a third ventricle cannula. Body temperature responses were monitored at 30 min intervals using colonic thermistor probes. Arginine vasopressin (AVP) level in the ventral septal area (VSA) determined by radioimmunoassay. RESULTS: In normal saline controls, rats were handled to take the colonic temperature, their body temperature significantly increased with a peak of (0.88?0.31)℃. The injection (icv) of ?-helical CRH(9-41), a CRH-41 receptor antagonists, markedly attenuated the stress-induced hyperthermia within 90 min after injection of normal saline. LPS(300 ng, icv) stimulated a biphasic rise in the colonic temperature, the 3.5 h thermal response index (TRI 3.5 ) and AVP levels in the VSA of LPS-treated rats were higher than those of control rats. The AVP responses to LPS were inhibited significantly by blockade of central CRH actions using ?-helical CRH(9-41) (5 ?g ,icv) administered 10 min prior to LPS, while ?-helical CRH(9-41) (5 ?g ,icv) resulted in exacerbated febrile responses to LPS(300 ng, icv). CONCLUSION: Central CRH plays an important role in stress-induced hyperthermia. The injection (icv) of ?-helical CRH(9-41) enhances markedly LPS-induced fever in rats. CRH is a dual action molecule in LPS-induced fever, which itself mediates LPS-induced fever, at the same time, and limits the rise in body temperature during fever through actions of AVP in the VSA and glucocoticoids.
