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NEURONAL ACETYLCHOLINE RECEPTOR MECHANISMS

NEURONAL ACETYLCHOLINE RECEPTOR MECHANISMS
神经元乙酰胆碱受体机制
批准号:
2685658
负责人:
Joseph F. Margiotta
金额:
$26.49万
依托单位国家:
美国
项目类别:
财政年份:
1994
资助国家:
美国
项目状态:
已结题
起止时间:
1994-01-01 至 2000-03-31

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项目成果

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中文摘要
翻译
描述:(改编自申请者摘要)对雏鸟的研究 睫状神经节的电生理、分子和显微研究 提出了检验两个假说的技术。一种假设是 突触外AChRs影响神经元存活的程度和 在发育过程中成熟。 第二种假设是,与ACh释放有关的突触前AChRs, 受神经肽产生的信号影响,从而提供一种 调节神经末梢释放的手段。 此外,在睫状神经节神经元中还发现了α7 AChR 相同神经元上的突触A3AChRs。马乔塔博士建议 通过测量A7来研究A7亚基在发育中的作用 在发育过程中的记录,测试 Achr阻断神经元存活、成熟和突触形成。 突触前AChRs将在培养的和新鲜的终末寻找 分离神经元并检测其对ACh释放的影响。至 检查突触和突触前AChR是否被不同的 细胞内信号,激活的亚型特异性效应 然后将阐明神经肽的不同信号通路。
英文摘要
DESCRIPTION: (adapted from Applicant's Abstract) Studies of the chick ciliary ganglion using electrophysiological, molecular, and microscopic techniques are proposed to test two hypotheses. One hypothesis is that extrasynaptic AChRs influence the extent of neuronal survival and maturation during development. A second hypothesis is that presynaptic AChRs, implicated in ACh release, are influenced by neuropeptide-generated signals thereby providing a means of modulating release from nerve terminals. Alpha7 AChRs have been found in ciliary ganglion neurons in addition to synaptic a3 AChRs on the same neurons. Dr. Margiotta proposes to investigate the role of a7 subunits in development by measuring a7 transcripts during the course of development, testing the effects of AChR blockade on neuron survival, maturation, and synapse formation. Presynaptic AChRs will be sought on terminals of cultured and freshly isolated neurons and tested for their effects on ACh release. To examine if synaptic and presynaptic AChRs are targeted by different intracellular signals, the subtype-specific effects of activating separate signaling pathways by neuropeptides will then be elucidated.
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Altering gene expression and function at single neuronal nicotinic synapses
Altering gene expression and function at single neuronal nicotinic synapses
NEURONAL ACETYLCHOLINE RECEPTOR MECHANISMS
NEURONAL ACETYLCHOLINE RECEPTOR MECHANISMS
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