Autonomic microganglion cells: a source of acetylcholine in the rat carotid body.

Autonomic microganglion cells: a source of acetylcholine in the rat carotid body.
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自主微神经节细胞:大鼠颈动脉体中乙酰胆碱的来源。

DOI:
10.1152/japplphysiol.00897.2003
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发表时间:
2004
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Marshall,Cathleen
Marshall,Cathleen
中科院分区:
--
文献类型:
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作者:
Gauda,EstelleB;Cooper,Reed;Johnson,ShereeM;McLemore,GabrielleL;Marshall,Cathleen

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外周动脉化学感受器的低氧化学敏感性和对氧气剥夺的呼吸反应随着出生后的发育而增加。在颈动脉小体(CB)合成的多种可能的神经递质被认为介导了缺氧产生的信号。乙酰胆碱(ACh)被认为是参与低氧化疗敏感性的主要兴奋性神经递质。然而,ACh是否起源于CB中的I型细胞尚不清楚。在这些研究中,我们验证了胆碱乙酰转移酶(ChAT)和囊泡性ACh转运体(Vacht)mRNAs在CB中表达的假设,以及随着出生后成熟或暴露在低氧中,mRNA水平会增加的假设。用半定量原位杂交组织化学和免疫组织化学方法对大鼠颈上神经节、结状-岩-颈静脉神经节复合体和颈上神经节的胆碱能标记进行定位。我们发现,两种ACh标记物在组织切片中的分布模式相似;然而,Vacht mRNA的水平一致高于ChAT。在结状-岩-颈静脉神经节复合体中,Vacht mRNA和免疫反应阳性物质大量存在于分布于CB的神经纤维中的多个微神经节细胞中,而ChAT mRNA仅在其中少数细胞中检测到。与我们的假设相反,出生后成熟导致ACh性状表达的减少,而低氧暴露并没有诱导CB、微神经节或神经节复合体中Vacht和ChAT mRNA水平的上调。本研究结果提示,丘脑ACh的来源可能是自主神经微节细胞和胆碱能神经末梢。
Hypoxic chemosensitivity of peripheral arterial chemoreceptors and the ventilatory response to O2deprivation increases with postnatal development. Multiple putative neurotransmitters, which are synthesized in the carotid body (CB), are thought to mediate signals generated by hypoxia. Acetylcholine (ACh) is believed to be a major excitatory neurotransmitter participating in hypoxic chemosensitivity. However, it is not known whether ACh originates from type I cells in the CB. In these studies, we tested the hypothesis that choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) mRNAs are expressed in the CB and that mRNA levels would increase with postnatal maturation or exposure to hypoxia. Semiquantitative in situ hybridization histochemistry and immunohistochemistry were used to localize cholinergic markers within neurons and cells of the rat CB, the nodose-petrosal-jugular ganglion complex, and the superior cervical ganglion up to postnatalday 28. We show that the pattern of distribution, in tissue sections, is similar for both ACh markers; however, the level of VAChT mRNA is uniformly greater than that of ChAT. VAChT mRNA and immunoreactivity are detected abundantly in the nodose-petrosal-jugular ganglion complex in a number of microganglion cells embedded in nerve fibers innervating the CB for all postnatal groups, whereas ChAT mRNA is detected in only a few of these cells. Contrary to our hypothesis, postnatal maturation caused a reduction in ACh trait expression, whereas hypoxic exposure did not induce the upregulation of VAChT and ChAT mRNA levels in the CB, microganglion, or within the ganglion complex. The present findings indicate that the source of ACh in the CB is likely within autonomic microganglion cells and cholinergic nerve terminals.