ANATOMY OF NEUROENDOCRINE PEPTIDE PATHWAYS IN BRAIN

描述：(直接取自应用程序)。促肾上腺皮质激素 驱动脑下-肾上腺对压力的反应。慢性肾衰也广泛存在于 脑下垂体-肾上腺对压力的反应。CRF也广泛表达在 通常调用的互补的自主和行为机制 通常在以下情况下调用的自主和行为机制 功能性CRF受体(CRF-R)提供了一种关键工具，用于 功能性CRF受体(CRF-R)提供了一个重要的工具，通过它 脑下垂体的分布与主要神经内分泌完全相容 在脑下垂体中的分布与大脑皮层的 包含突起，特别是在牵涉到压力的区域- 含有CRF的投射，特别是在被牵连的区域 确定并提供功能解剖学背景，用于 旨在识别和提供功能解剖学背景 关于如何协调地区差异的替代假设 寻求关于差异可能有多大的替代假设 和电子显微镜水平来表征细胞和亚细胞 将在光学和电子显微镜水平上用来表征 脑下垂体促肾上腺皮质激素。双重染色方法将评估 脑组织CRF和脑垂体促肾上腺皮质激素的表达。双重染色 与CRF-R-ir的突触后膜特化相反 突触终末可能与突触后膜相对应 将首先使用mRNA和/或蛋白质的表达来确定 感兴趣的区域。各种原位检测mRNA和/或蛋白质的方法 环境，调节CRF内外表达的主要因素 糖皮质激素环境中的应激和扰动 在脑和垂体中有和不有CRF靶细胞中进行处理 下丘脑。CRF-R被隔离和处理的方式 将在光镜和电子显微镜水平上进行探索 另一个高亲和力CRF结合部分，CRF结合蛋白将 杂交组织化学方法，就像刚才描述的 挑战条件。最后，我们将使用免疫和杂交技术 通过新的配体调节CRF-R和/或存在 明显的配基-受体失配的主要区域可能通过 正在处理变体或子类型。滴度和/或变化 下丘脑外CRF可导致库辛戈德或艾迪生症状， 对库辛戈德或艾迪生症状的改良免疫易感性 神经性厌食症、重度厌食症等情感性精神障碍的病因 神经性厌食症和重度抑郁症等疾病。集体地 促肾上腺皮质激素释放因子信号传导的神经内分泌和神经生物学背景 CRF在多个水平上的信号传导的神经生物学背景 应激相关的神经和神经内分泌系统。

Description: (Taken directly from the application). Corticotropin- driving pituitary-adrenal responses to stress. CRF is also widely pituitary-adrenal responses to stress. CRF is also widely expressed in complementary autonomic and behavioral mechanisms that are commonly invoked autonomic and behavioral mechanisms that are commonly invoked following of a functional CRF receptor (CRF-R) provides a critical tool with which to a functional CRF receptor (CRF-R) provides a critical tool with which distribution in pituitary is fully compatible with the major neuroendocrine distribution in pituitary is fully compatible with the major containing projections, particularly in regions implicated as stress- of CRF-containing projections particularly in regions implicated as identifying, and providing a functional anatomical context, for areas in aimed at identifying and providing a functional anatomical context for alternative hypotheses as to how discrepancies may be reconciled in regions to pursue alternative hypotheses as to how discrepancies may be and electron microscopic level to characterize the cellular and subcellular will be used at the light and electron microscopic level to characterize corticotropin in pituitary. Dual staining approaches will assess those of CRF in brain and of corticotropin in pituitary. Dual staining apposed to postsynaptic membrane specializations with which CRF-R-ir is terminals may be synaptically apposed to postsynaptic membrane of mRNA and/or protein expression will be employed to determine first how regions of interest. Various in situ assays of mRNA and/or protein environment, the major factors modulating CRF expression within and beyond stress and perturbations in the corticosteroid environment the major processed in CRF target cells in brain and pituitary that do and do not hypothalamus. The manner in which CRF-R is sequestered and processed in will be explored at the light and electron microscopic levels under basal another high-affinity CRF-binding moiety the CRF- binding protein will hybridization histochemical approaches like those just described to challenged conditions. Finally we will employ immuno- and hybridization accommodated by novel ligands for the CRF-R and/or the existence of major areas of apparent ligand-receptor mismatch may be accommodated by processing variants or subtypes. Alterations in titers and/or extrahypothalamic CRF can lead to Cushingoid or Addisonian symptoms, to Cushingoid or Addisonian symptoms modified susceptibility to immune the etiology of affective disorders such as anorexia nervosa and major disorders such as anorexia nervosa and major depression. Collectively neuroendocrine and neurobiological contexts for signaling by CRF at neurobiological contexts for signaling by CRF at multiple levels of stress-related neuronal and neuroendocrine systems.