Jamen F, Alonso G, Shibuya I, Widmer H, Vacher C-M, Calas A, Bockaert J, Brabet P, Dayanithi G
UPR 9023-CNRS and UMR 5101-CNRS, CCIPE, Montpellier, France.
J Neuroendocrinol. 2003 Sep;15(9):871-81. doi: 10.1046/j.1365-2826.2003.01075.x.
The role of pituitary adenylate cyclase-activating polypeptide (PACAP) type I receptor (PAC1 receptor) in regulating hypothalamic supraoptic neurones was investigated using PAC1 receptor-deficient male mice (PAC1-/-). The effects of PACAP on [Ca2+]i were investigated in freshly dissociated supraoptic neurones and on the somatodendritic release of vasopressin and oxytocin, examined on intact supraoptic nuclei. In supraoptic neurones from wild-type mice (PAC1+/+), 100 nm PACAP induced an increase in [Ca2+]i and release of vasopressin and oxytocin, whereas in heterozygous (PAC1+/-) and null-mutant mice (PAC1-/-), PACAP was much less effective. PACAP had no effect on these two parameters when applied to isolated neurohypophysial nerve terminals of PAC1+/+ and PAC1-/- mice, and rats. In conclusion, the PAC1 receptor is solely responsible for the PACAP-induced [Ca2+]i signalling and secretion of vasopressin and oxytocin in the somatodendritic region of supraoptic neurones.
利用垂体腺苷酸环化酶激活多肽（PACAP）I型受体（PAC1受体）缺陷雄性小鼠（PAC1-/-），研究了PAC1受体在调节下丘脑视上核神经元中的作用。在新鲜分离的视上核神经元中研究了PACAP对[Ca2+]i的影响，并在完整的视上核上检测了PACAP对血管加压素和催产素树突-胞体释放的影响。在野生型小鼠（PAC1+/+）的视上核神经元中，100 nM PACAP可诱导[Ca2+]i增加以及血管加压素和催产素释放，而在杂合子（PAC1+/-）和纯合突变小鼠（PAC1-/-）中，PACAP的作用则弱得多。将PACAP应用于PAC1+/+和PAC1-/-小鼠以及大鼠的离体神经垂体神经末梢时，对这两个参数均无影响。总之，PAC1受体是视上核神经元树突-胞体区域中PACAP诱导的[Ca2+]i信号转导以及血管加压素和催产素分泌的唯一原因。
