首页> 外文期刊>The Journal of Comparative Neurology >Transient receptor potential vanilloid type 4 is expressed in vasopressinergic neurons within the magnocellular subdivision of the rat paraventricular nucleus of the hypothalamus
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Transient receptor potential vanilloid type 4 is expressed in vasopressinergic neurons within the magnocellular subdivision of the rat paraventricular nucleus of the hypothalamus

机译:瞬态受体潜在的香草型4在丘脑腺内核心细胞核的甲状腺细胞细胞内表达,在丘脑盆腔的甲状腺细胞内

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Abstract Changes in plasma osmolality can drive changes in the output from brain centres known to control cardiovascular homeostasis, such as the paraventricular nucleus of the hypothalamus (PVN). Within the PVN hypotonicity reduces the firing rate of parvocellular neurons, a neuronal pool known to be involved in modulating sympathetic vasomotor tone. Also present in the PVN is the transient receptor potential vanilloid type 4 (TRPV4) ion channel. Activation of TRPV4 within the PVN mimics the reduction in firing rate of the parvocellular neurons but it is unknown if these neurons express the channel. We used neuronal tracing and immunohistochemistry to investigate which neurons expressed the TRPV4 ion channel protein and its relationship with neurons known to play a role in plasma volume regulation. Spinally projecting preautonomic neurons within the PVN were labelled after spinal cord injection of FluoroGold (FG). This was followed by immunolabelling with anti‐TRPV4 antibody in combination with either anti‐oxytocin (OXT) or anti‐vasopressin (AVP). The TRPV4 ion channel was expressed on 63% of the vasopressinergic magnocellular neurosecretory cells found predominantly within the posterior magnocellular division of the PVN. Oxytocinergic neurons and FG labelled preautonomic neurons were present in the same location, but were distinct from the TRPV4/vasopressin expressing neurons. Vasopressinergic neurons within the supraoptic nucleus (SON) were also found to express TRPV4 and the fibres extending between the SON and PVN. In conclusion within the PVN, TRPV4 is well placed to respond to changes in osmolality by regulating vasopressin secretion, which in turn influences sympathetic output via preautonomic neurons.
机译:摘要血浆渗透压的变化可以驱动已知的脑中中心的输出的变化,该脑中心控制心血管稳态,例如下丘脑(PVN)的椎间盘核。在PVN中,低渗性降低了细胞内神经元的烧制率,已知称为调节交感神经调制调制的神经元池。还存在于PVN中的是瞬态受体电位试用型4(TRPV4)离子通道。 PVN内的TRPV4的激活模仿细胞内神经元的烧制率的降低,但如果这些神经元表达通道,则是未知的。我们使用神经元跟踪和免疫组织化学来研究哪种神经元表达TRPV4离子通道蛋白及其与已知在血浆体积调节中作用作用的神经元的关系。在荧光帘线(FG)的脊髓注入后,PVN内的专业神经元脊髓突出的神经元。然后通过与抗催产素(OXT)或抗血管加压素(AVP)组合的抗TRPV4抗体免疫标注。 TRPV4离子通道在63%的血管连接胶质细胞神经细胞中表达,主要在PVN的后甲型粒细胞内发现。催产剂神经元和FG标记的专业神经元存在于同一位置,但与表达神经元的TRPV4 / VasoPressin不同。还发现上升核(儿子)内的血管加压素神经元表达TRPV4和在儿子和PVN之间延伸的纤维。总之,通过调节血管加压素分泌,TRPV4良好地求响应渗透性的变化,这反过来影响通过非专利神经元的交感神经输出。

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