CA2+ CHANNELS IN SYMPATHETIC NEURONS

交感神经元中的 CA2 通道

• 批准号: 2714565
• 负责人: Ann R. Rittenhouse
• 金额: $ 10.91万
• 依托单位: UNIV OF MASSACHUSETTS MED SCH WORCESTER
• 依托单位国家: 美国
• 财政年份: 1995
• 资助国家: 美国
• 起止时间: 1995-06-01 至 2000-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2714565
• 关键词: G protein; PC12 cells; action potentials; calcium channel; calcium channel blockers; complementary DNA; dihydropyridines; insect poison; laboratory rat; neural plasticity; neuropharmacology; neurotoxins; neurotransmitters; northern blottings; nucleic acid sequence; phosphatase inhibitor; phosphorylation; protein structure function; sympathetic ganglion; voltage gated channel

DESCRIPTION: (adapted from Applicant's Abstract) The long-term goal of the experiments described in this proposal is to identify sources of plasticity of voltage-activated calcium (Ca) channels. The N-type Ca channel has been found only in nerve cells and neuronally-derived tissues, is associated with the regulation of neurotransmitter synthesis and release from presynaptic nerve endings, and in turn, is modulated by many of these same neurotransmitters. N-type Ca channels are the most highly modulated Ca channel in the brain in that more pathways exist for modulation of this Ca channel than for any other, and because of this, are thought to play a special role in the brain. N-type Ca channels display endogeous, heterogeneous activity, called modes, where measured unitary conductance and kinetics vary from mode to mode. Each mode can last for seconds to minutes. At least six modes have been identified and are a source of neural plasticity at the level of the N-type Ca channel. The specific aims of this project are to 1) identify the causes of modal gating and permeation of N-type Ca currents that give rise to channel plasticity, 2) determine whether modulation of N-type Ca channel behavior by neurotransmitters and cellular signals alters the frequency of occurrence and/or the biophysical characteristics of these modes, and 3) identify differences between the subunit composition of N-type Ca channels in sympathetic neurons and in the brain and determine whether differences in the expression level of the subunits is an additional source of plasticity.

描述：（改编自申请人的摘要）长期目标 本提案中描述的实验是为了确定 电压激活钙 (Ca) 通道的可塑性。 N型钙 通道仅在神经细胞和神经元衍生的细胞中发现 组织，与神经递质合成的调节有关 并从突触前神经末梢释放，反过来又受到调节 由许多相同的神经递质。 N型Ca通道最多 大脑中高度调节的 Ca 通道，存在更多通路 该 Ca 通道的调制程度高于任何其他通道，因此， 被认为在大脑中发挥着特殊作用。 N型Ca通道 显示内源的、异质的活动，称为模式，在测量时 单一电导和动力学因模式而异。 每种模式都可以 持续几秒到几分钟。 至少已确定六种模式 是 N 型 Ca 通道水平神经可塑性的来源。 该项目的具体目标是 1）确定模态的原因 产生通道的 N 型 Ca 电流的门控和渗透 可塑性，2）判断是否调制N型Ca通道 神经递质和细胞信号的行为改变频率 这些模式的发生和/或生物物理特征，以及 3) 识别N型Ca亚基组成之间的差异 交感神经元和大脑中的通道并确定是否 亚基表达水平的差异是一个额外的因素 可塑性的来源。