Cytochemical observations of Neuronal Influence on Vasopressin Synthesis and secretion

神经元对加压素合成和分泌影响的细胞化学观察

基本信息

批准号：
02670019
负责人：
NAKAI Yasumitsu
金额：
$ 1.54万
依托单位：
Showa University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1991
项目状态：
已结题

项目摘要

Synaptic inputs of noradrenaline- and brain natriuretic peptide-containing terminals to arginine-vasopressin producing cells(AVP cells)were observed, respectively, in the supraoptic and paraventricular nuclei(SON, PVN)of the rat hypothalamus using double immunostaining. In addition, axon terminals orginated from the neurons in the Al/Cl cell group in the medulla oblongata have been found to make synapses with AVP cells in the PVN and the SON using a double labeling technique combining WGA-HRP anterograde tracing with AVP immunocytochemistry at electron microscopic level.Using in situ hybridization and immunocytochemistry, we ekamined neuronal influence on vasopressin(AVP)-gene expression in rat hypothalamus after unilateral electrolytic lesion of the ventrolateral medulla, containing catecholaminergic neurons forming the Al cell group. Because Al neurons are throught to be the source of noradrenergic terminals upon the magnocellular neurons that release AVP dominantly.In the normal con … More trol rat, there was no difference in AVP-MRNA levels in magnocellular neurons between, the PVN and SON nuclei. However, unilateral Allesion caused AVP-MRNA levels between the normal and the lesioned rats. Furthermore, stimulation of water-deprivation in the lesioned rat increased in AVP-mRNA levels significantly not only in the SON but also in the PVN. I these experiments, there was no significant difference in rat plasma osmolarity and electrolytes(Na^+, K^+, Ca^<++>)(p<0.05).These results indicate that the AVP-gene expression in rat magnocellular neurons in differentially influenced between the PVN and SON by the neuronal regulation through the ventrolateral medulla, and at least in part, some pathways may through Al area to contribute to increase in levels in the PVN. Moreover, it is clarified that Al lesion does not inhibit the response of waterdeprivation in magnocellular neurons in both nuclei, suggesting deprovation in magnocellular neurosecretory neurons in both nuclei, suggesting different pathways and different mechanisms concerning to the AVP-gene expression. Less

在上丘脑和脑室性核（SON，PVN）中，分别观察到甲肾上腺素和脑纳他蛋白肽的突触输入到精氨酸 - 毒素产生细胞（AVP细胞）的突触输入。 In addition, axon terminals ordered from the neurons in the Al/Cl cell group in the medulla oblongata have been found to make synapses with AVP cells in the PVN and the SON using a double labeling technique combining WGA-HRP anterograde tracing with AVP immunocytochemistry at electronic microscopic level.Using in situ hybridization and immunocytochemistry, we etched神经元对腹侧髓质单侧电解病变后大鼠下丘脑中加压素（AVP） - 元的影响，其中包含形成Al细胞组的Catecholamin能神经元。因为AL神经元在磁性神经元上主要释放AVP的北肾上腺末端。然而，单侧的差距导致正常大鼠和病变的大鼠之间的AVP-MRNA水平。此外，在病变大鼠中，AVP-MRNA水平的刺激不仅在SON中而且在PVN中也显着增加。 i这些实验，大鼠血浆渗透压和电解质没有显着差异（Na^+，K^+，Ca^<++>）（P <0.05）。这些结果表明，通过腹侧髓质通过神经元调节在PVN和SON之间差异影响的大鼠磁神经元中的AVP基因表达，至少部分地，某些途径可能通过Al区域来促进PVN的水平增加。此外，可以澄清的是，AL病变不会抑制核元中磁神经元中水剥落的反应，这表明两个核中磁神经递归神经元中的剥夺，表明不同的途径和有关AVP基因表达的不同途径和不同的机制。较少的