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CELLULAR MECHANISMS OF INFORMATION PROCESSING IN NEURONS

神经元信息处理的细胞机制

基本信息

批准号：
6539953
负责人：
COSTA M COLBERT
金额：
$ 10.6万
依托单位：
UNIVERSITY OF HOUSTON
依托单位国家：
美国
项目类别：
财政年份：
1998
资助国家：
美国
起止时间：
1998-09-01 至 2004-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6539953
关键词：
GABA receptor action potentials axon dendrites laboratory rat neural information processing neurons potassium channel sodium channel soma voltage /patch clamp

项目摘要

DESCRIPTION The overall goal of the proposed research is to understand the cellular mechanisms that underlie the processing of information by single neurons. A key step in this processing is the conversion of membrane potential into action potentials. Recent work in pyramidal neurons suggests that, due to a low threshold, initiation of action potentials occurs in the axon. What determines this threshold, however, is not understood. The first hypothesis to be tested is that the threshold for action potential initiation is lower in the axon than in the soma because the density of Na+ channels is high and the density of A-type channels is low in the axon. The Specific Aims are 1) To determine and compare the relative densities and biophysical parameters of Na+ and K+ channels in the axon and soma using patch-clamp techniques and 2) to determine which channels are major determinants of threshold in the axon by manipulating threshold pharmacologically during whole-cell recording. The second hypothesis is that inhibitory synapses on the initial segment increase action potential threshold by decreasing current flow to the site of initiation in the axon. The Specific Aims are to 3) determine the voltage drop between the soma and axon and to measure thresholds with and without activation of GABAA receptors on the initial segment, and 4) to determine if the site of action potential initiation shifts to the dendrites when the threshold is raised by activation of GABAA receptors on the initial segment and soma. These studies will provide much needed data on the cellular mechanisms underlying action potential initiation and its modulation.

描述拟议研究的总体目标是了解细胞单个神经元处理信息的基本机制。一这个过程中的关键步骤是将膜电位转化为动作电位最近对锥体神经元的研究表明，低阈值，动作电位的起始发生在轴突中。什么然而，这个阈值的确定并不清楚。第一种假设要测试的是，动作电位启动的阈值较低，在轴突中比在索马中更高，因为Na+通道的密度高，轴突中A型通道密度低。具体目标是：（1）确定和比较相对密度和生物物理参数用膜片钳技术观察轴突和索马中Na+和K+通道的变化， 2)为了确定哪些通道是阈值的主要决定因素，在全细胞过程中通过操纵阈值放大来调节轴突录制. 第二个假设是，通过降低电流来增加动作电位阈值，轴突中的起始位点。具体目标是：（3）确定索马和轴突之间的电压降，并且在起始节段上没有GABAA受体的活化，以及4）确定动作电位起始部位是否转移到树突当阈值通过激活初始的GABAA受体而升高时，节和索马。这些研究将提供急需的数据动作电位起始的细胞机制及其调变

项目成果

期刊论文数量（5）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Arachidonic acid reciprocally alters the availability of transient and sustained dendritic K(+) channels in hippocampal CA1 pyramidal neurons.

花生四烯酸相互改变海马 CA1 锥体神经元中瞬时和持续树突 K( ) 通道的可用性。

DOI：
10.1523/jneurosci.19-19-08163.1999
发表时间：
1999
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
0
作者：
Colbert,CM;Pan,E
通讯作者：
Pan,E

Subthreshold inactivation of Na+ and K+ channels supports activity-dependent enhancement of back-propagating action potentials in hippocampal CA1.

Na 和 K 通道的阈下失活支持海马 CA1 中反向传播动作电位的活动依赖性增强。