コルチコトロピン放出因子のラット脳室内投与は脳内グルタミン酸受容体を介してラット排尿を促進する

抄録

Roles of brain corticotropin-releasing factor (CRF), a representative stress-related neuropeptide, on micturition reflex are controversial, both suppressive and facilitatory roles are reported. In this study, we examined effects of intracerebroventricularly (icv) administered CRF on micturition reflex in urethane-anesthetized (0.8 g/kg, ip) male Wistar rats (300-450 g). A catheter was inserted into the bladder to perform cystometry. Three hours after the surgery, CRF (1 or 3 nmol/rat) was icv administered. Effects of icv pretreated CP154526 (CP, CRF1 receptor antagonist, 30 or 100 nmol/rat), K41498 (K, CRF2 receptor antagonist, 30 nmol/rat), MK-801 (MK, NMDA receptor antagonist, 3 or 10 nmol/rat) or DNQX (AMPA receptor antagonist, 1 or 3 nmol/rat) on the CRF-induced responses were also examined. CRF dose-dependently shortened intercontraction intervals (ICI), an index of micturition frequency. The CRF-induced ICI shortening was significantly attenuated by icv pretreated CP, MK or DNQX, respectively. On the other hand, K showed no significant effect on the CRF-induced response. These results suggest that brain CRF can facilitate the micturition reflex via brain NMDA/AMPA glutamatergic receptors in rats.