抄録
The effect of corticotrophin-releasing factor (CRF) on oxytocin (OT) mRNA expressing neurons in the rat paraventricular nucleus (PVN) was examined using whole-cell patch-clamp recordings and single-cell reverse transcription-polymerase chain reaction (SC-RT-PCR) technique. Under current-clamp, CRF (10 nM to 600 nM) resulted in increased basal firing rate and depolarization while decreased the amplitude of the afterhyperpolarization (AHP) in a dose-dependent manner. CRF-induced depolarization was unaffected by co-perfusion with 0.5 μM tetrodotoxin (TTX) + 10 μM CNQX + 10 μM bicuculline. Under voltage-clamp, 100-600 nM CRF significant reduced the apamin-sensitive slow Ca2+-dependent K+ current (IAHP), while increased the ZD-7288-sensitive hyperpolarization-activated cation current (IH). Extracellular application of 1 μM α-helical CRF-(9-14) (α-h CRF), a selective CRF receptors antagonist, completely blocked the CRF-induced effects in both current- and voltage-clamp. And the SC-RT-PCR analysis indicated that all the OT mRNA-expressing neurons co-expressed CRF receptor 1 mRNA and CRF receptor 2 mRNA. These results suggest that OT mRNA expressing neurons co-express CRF receptors mRNA, and CRF combined to CRF receptors, depolarizes these neurons via inhibits IAHP and enhances IH channel activities. [Jpn J Physiol 54 Suppl:S198 (2004)]
