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ADENOSINE DERIVATIVES AND TRANSMITTER RELEASE

ADENOSINE DERIVATIVES AND TRANSMITTER RELEASE
腺苷衍生物和递质释放
批准号:
3394981
负责人:
EUGENE M SILINSKY
金额:
$16.3万
依托单位国家:
美国
项目类别:
财政年份:
1979
资助国家:
美国
项目状态:
已结题
起止时间:
1979-05-01 至 1994-11-30

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中文摘要
翻译
这项研究的总体目标是进一步了解 递质释放的机制及其腺苷的调节 衍生物. 在下一个支持期间,计划使用 电生理学,发光和脂质体为基础的方法来研究 脊椎动物嘌呤能传递的四个方面 外周神经系统:1)我们将进一步研究腺苷受体如何在外周神经系统中发挥作用。 激活被转换为乙酰胆碱(ACh)的抑制 运动神经末梢的分泌物。 腺苷是否通过抑制乙酰胆碱的释放 减少Ca通过电压门控膜通道进入或损害 细胞内的行动钙?2)我们将研究腺苷在 刺激量子发射器释放 两种负责的受体 增加递质释放和潜在的机制 将研究腺苷对哺乳动物运动神经刺激作用 在哺乳动物的粘膜下神经丛中的终末和神经末梢 肠神经系统。3)我们将调查ATP 可能是粘膜下神经丛的兴奋性神经递质。 两者 ATP衍生物的突触后效应和钙依赖性释放 ATP将被研究。4)我们会调查 腺苷是外周突触可塑性的调节剂,反映为 青蛙交感神经链神经节的长时程增强。 腺苷及其同类物通过作用于突触连接, 被认为是许多生理学的天然介质, 行为和病理过程。 研究了 腺苷在脊椎动物的某些部位发挥其生理作用 神经系统,允许精确的电生理测量 分泌物很可能提供有用的基本信息, 嘌呤调节神经元行为的机制。
英文摘要
The overall objective of this research,is to further our knowledge of the mechanisms of transmitter release and its modulation by adenosine derivatives. For this next period of support,it is intended to use electrophysiological,luminometric and liposome-based methods to study the following four aspects of purinergic transmission in the vertebrate peripheral nervous system:1) We will study further how adenosine receptor activation is transduced into the inhibition of acetylcholine (ACh) secretion at motor nerve endings. Does adenosine inhibit ACh release by reducing Ca entry through voltage-gated membrane channels or impair the intracellular actions of Ca? 2) We will study the effects of adenosine in stimulating quantal transmitter release. Both the receptors responsible for increasing transmitter release and the mechanisms underlying the stimulatory effect of adenosine will be studied at mammalian motor nerve terminals and at nerve endings in submucous plexus of the mammalian enteric nervous system. 3) We will investigate the possibility that ATP may be an excitatory neurotransmitter in the submucous plexus. Both the postsynaptic effects of ATP derivatives and the calcium-dependent release of ATP will be studied. 4) We will investigate the possibility that adenosine is a modulator of peripheral synaptic plasticity reflected as long-term potentiation in frog sympathetic chain ganglia. Adenosine and its congeners,by their actions on synaptic junctions,have been implicated as natural mediators of a number of physiological, behavioral and pathological processes. Studying the mechanisms by which adenosine exerts its physiological effects at sites in the vertebrate nervous system that allow accurate electrophysiological measurements of secretions is likely to provide useful basic information on the underlying mechanisms by which purines regulate neuronal behavior.
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