VASOPRESSIN/OXYTOCIN AND THE CONTROL OF ACTH RELEASE
VASOPRESSIN/OXYTOCIN AND THE CONTROL OF ACTH RELEASE
批准号:
3417171
负责人:
Craig F Ferris
金额:
$13.15万
依托单位国家:
美国
项目类别:
财政年份:
1992
资助国家:
美国
项目状态:
已结题
起止时间:
1992-07-01 至 1995-06-30
关键词:
adrenocorticotropic hormone aggression biological models blood circulation cold temperature corticotropin releasing factor cortisol hamsters hormone regulation /control mechanism hypoglycemia immunocytochemistry in situ hybridization long term potentiation microinjections neuroendocrine system neurohypophysis oxytocin physiologic stressor pituitary gland radioimmunoassay respiratory distress syndrome of newborn secretion stress vasopressins
中文摘要
垂体前叶促肾上腺皮质激素的释放增加,
压力刺激在很大程度上取决于协同效应。
促肾上腺皮质激素释放激素(CRH)、加压素(VP)和
催产素(OXY)。 与VP共定位的小细胞神经元的激活
和CRH,并终止于正中隆起的外带,
被认为是应激诱发释放的主要神经内分泌途径。
促肾上腺皮质激素 然而,有证据表明巨细胞VP和OXY系统,
其纤维穿过正中隆起的内部区域,
终止于神经垂体,可能有助于测量VP和OXY
在门静脉循环,并加强CRH诱导的ACTH
在压力下释放。 到目前为止,还没有实验模型
这将使小细胞系统的研究独立于
巨细胞系统 然而,人们发现,
通过显微注射自杀药物,
将凝集素Volkensin转运到神经垂体。 有了这个新模型
我们将研究大细胞VP和OXY的功能意义
系统在应激期间ACTH释放的控制中的作用:(1)比较
微量注射VP和OXY的仓鼠门脉循环中的VP和OXY水平
用volkensin或生理盐水载体进入神经垂体,和(2)
比较两组患者的ACTH、皮质醇、VP和OXY水平,
微注射沃肯辛或盐水载体的仓鼠的循环
对以下因素的反应:(A)短暂暴露于乙醚,(B)胰岛素诱导
低血糖,(C)暴露于低环境温度,和(D)侵袭性
同类之间的相遇 这些研究将提供一个独特的
有机会研究小细胞之间的功能相互作用,
大细胞系统在ACTH神经内分泌调节中的作用
分泌,并应加强我们对神经组织的理解,
CRH、VP和OXY神经元的激活和相互作用,
压力下的适应性反应
英文摘要
The heightened release of ACTH from th anterior pituitary in response to
stressful stimuli is, in a large part, dependent upon the synergistic
actions of corticotropin-releasing hormone (CRH), vasopressin (VP), and
oxytocin (OXY). The activation of parvocellular neurons that colocalize VP
and CRH and terminate in the external zone of the median eminence is
thought to be the major neuroendocrine pathway for stress-evoked release of
ACTH. However, there is evidence that the magnocellular VP and OXY system,
whose fibers pass through the internal zone of the median eminence to
terminate in the neurohypophysis, may contribute to the VP and OXY measured
in the portal circulation, and to the potentiation of CRH-induced ACTH
release during stress. Until now, there has been no experimental model
that would allow the parvocellular system to be studied independent of the
magnocellular system. However, it was discovered that the magnocellular
system can be eliminated in hamsters by microinjecting the suicide
transport lectin volkensin into the neurohypophysis. With this new model
we will examine the functional significance of the magnocellular VP and OXY
system in the control of ACTH release during stress by: (1) comparing the
levels of VP and OXY in the portal circulation in hamsters microinjected
into the neurohypophysis with volkensin or saline vehicle, and (2)
comparing the levels of ACTH, cortisol, VP and OXY in the systemic
circulation in hamsters microinjected with volkensin or saline vehicle in
response to: (A) brief exposure to ether, (B) insulin-induced
hypoglycemia, (C) exposure to low ambient temperatures, and (D) aggressive
encounters between conspecifics. These studies will provide a unique
opportunity to examine the functional interaction between the parvocellular
and magnocellular systems in the neuroendocrine regulation of ACTH
secretion, and should enhance our understanding of the neural organization,
activation, and interaction of CRH, VP, and OXY neurons that contribute to
adaptive responding during stress.
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