作者: Yoichi Ueta , Kaori Sato-Numata , Kaori Sato-Numata , Tomohiro Numata , Yasunobu Okada
DOI: 10.33594/000000342
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摘要: Background/aims Arginine vasopressin (AVP) neurons play an important role for sensing a change in the plasma osmolarity and thereby responding with regulated AVP secretion order to maintain body fluid homeostasis. The osmo-sensing processes magnocellular neurosecretory cells (MNCs) including oxytocin (OXT) of hypothalamus were reported be coupled sustained osmotic shrinkage or swelling without exhibiting discernible cell volume regulation. Since increasing evidence has shown some differences properties between OXT neurons, responses are reexamined distinguishing these types from each other. We previously that identified by transgenic expression enhanced green fluorescence protein (eGFP) possess ability regulatory decrease (RVD) after hypoosmotic swelling. Thus, present study, we examined increase (RVI) hyperosmotic neurons. Methods Here, used eGFP-identified acutely dissociated AVP-eGFP rats. performed single-cell size measurements, cytosolic RT-PCR analysis, patch-clamp studies. Results found respond challenge physiological caused massive AVP, called secretory (SVD), superimposed onto physical shrinkage, also exhibit RVI coping shrinkage. Furthermore, our pharmacological molecular examinations indicated its associated SVD event triggered activation T-type Ca2+ channels, is attained parallel operation Na+/H+ exchanger Cl-/HCO3- anion exchanger. Conclusion it concluded stimulation activating ion transporters respectively.