Physiology of Muscarinic Synapses in Sympathetic Ganglia

交感神经节毒蕈碱突触的生理学

基本信息

批准号：
7582362
负责人：
JOHN P HORN
金额：
$ 31.92万
依托单位：
UNIVERSITY OF PITTSBURGH AT PITTSBURGH
依托单位国家：
美国
项目类别：
财政年份：
1984
资助国家：
美国
起止时间：
1984-07-01 至 2011-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7582362
关键词：
Acetylcholine Adrenergic Agents Amphibia Amplifiers Anatomy Angiotensin II Receptor Architecture Autonomic ganglion B-Lymphocytes Behavior Biological Models Blood Pressure Body Temperature Cardiac Cardiovascular Physiology Cells Cervical Communication Computer Simulation Data Development Electrophysiology (science)Elements Experimental Models Feedback Functional disorder Ganglia Gland Goals Heart Rate Heart failure Human Hypertension Lateral Life Measurement Measures Mediating Methodology Methods Modeling Molecular Muscarinics Myocardium Myxoid cyst Neuroanatomy Neurons Neuropeptides Noise Norepinephrine Pathway interactions Phenotype Physiological Physiology Play Preparation Pressoreceptors Process Property Rana catesbeiana Rattus Regulation Research Role Scheme Shapes Signal Transduction Smooth Muscle Source Stimulus Structure of parasympathetic ganglion Structure of superior cervical ganglion Structure of thyroid parafollicular cell Sympathetic Ganglia Synapses Synaptic plasticity Syncope System Testing Time Tissues Training Varicosity Vasoconstrictor Agents Vasomotor Work adrenergic base cell type heart rhythm motor control neurophysiology noradrenergic novel presynaptic quantum receptor relating to nervous system research study virtual voltage voltage clamp

项目摘要

Sympathetic and parasympathetic ganglia provide the final common pathway for ail central motor control of smooth muscle, cardiac muscle and glands in tissues that mediate autonomic behavior. The long-term goals of this project are to determine how the neural architecture of autonomic ganglia enables them to transform spike trains, to elucidate how molecular and cellular mechanisms of synaptic plasticity shape this process, and to define the principles of ganglionic integration that contribute to behavior. The proposed work will focus upon modulatory muscarinic synapses in sympathetic ganglia, with emphasis on the subset of neurons that control cardiovascular function. The project will employ cellular neurophysiology, computational simulations, and neuroanatomy methods in two model systems - bullfrog sympathetic ganglia and the rat superior cervical sympathetic ganglion. Many of the physiological experiments will use the dynamic clamp method to implement virtual nicotinic synapses on living neurons and then determine how they interact with metabotropic neuromodulatory mechanisms. The analysis is predicated upon a working hypothesis that paravertebral sympathetic ganglia behave as variable synaptic amplifiers of activity whose gain is regulated by the strength and convergence of nicotinic synapses and by the expression of neuromodulatory mechanisms that serve to adjust the strength of nicotinic synapses. The specific aims are: 1) To contrast activity-dependent muscarinic gain modulation in three different sympathetic cell types. 2) To measure the contributions of quanta! noise and presynaptic plasticity to synaptic gain. 3) To analyze the regulation of ganglionic integration by cardiac rhythms. 4) To test the hypothesis that metabotropic signaling through muscarinic, alpha-adrenergic and angiotensin II receptors provides a basis for phenotypic specialization of ganglionic integration in the rat SCO. Concepts developed through this research will contribute to fundamental understanding of normal autonomic behavior and human pathophysiology, especially to changes associated with syncope, hypertension and heart failure.

交感神经和副交感神经神经节为ail中央电动机控制提供了最终的公共途径平滑肌，心肌和腺体介导自主行为的组织中。长期目标该项目的一个是确定自主神经节的神经结构如何使他们能够改变尖峰列车，以阐明突触可塑性的分子和细胞机制如何塑造此过程，并定义有助于行为的神经节整合原理。拟议的工作将着重于同情神经节中的调节性毒蕈碱突触，重点是神经元的子集控制心血管功能。该项目将采用细胞神经生理学，计算两个模型系统中的模拟和神经解剖学方法 - 牛蛙交感神经和大鼠宫颈上等交感神经节。许多生理实验将使用动态夹具在活神经元上实现虚拟烟碱突触，然后确定它们如何与之互动的方法代谢性神经调节机制。分析是基于一个工作假设的副交感神经节的行为作为可变的活动的突触放大器，其增益受调节通过烟碱突触的强度和收敛性和神经调节的表达用于调整烟碱突触强度的机制。具体目的是：1）对比在三种不同的交感细胞类型中，活动依赖性毒蕈碱增益调节。 2）测量 Quanta的贡献！噪声和突触前的可突触增益。 3）分析调节神经节融合通过心律。 4）测试通过代谢信号传导的假设毒蕈碱，α-肾上腺素和血管紧张素II受体为表型专业化提供了基础大鼠SCO中的神经节整合。通过这项研究发展的概念将有助于对正常自主行为和人类病理生理学的基本了解，尤其是与晕厥，高血压和心力衰竭相关的变化。

项目成果

期刊论文数量（20）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Role of ganglionic cotransmission in sympathetic control of the isolated bullfrog aorta.

神经节共传递在离体牛蛙主动脉交感神经控制中的作用。

DOI：
10.1113/jphysiol.1997.sp021851
发表时间：
1997
期刊：
The Journal of physiology
影响因子：
0
作者：
Thorne,R;Horn,JP
通讯作者：
Horn,JP

Preganglionic and sensory origins of calcitonin gene-related peptide-like and substance P-like immunoreactivities in bullfrog sympathetic ganglia.

牛蛙交感神经节降钙素基因相关肽样和 P 物质样免疫反应性的节前和感觉起源。

DOI：
10.1523/jneurosci.09-07-02543.1989
发表时间：
1989
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
0
作者：
Horn,JP;Stofer,WD
通讯作者：
Stofer,WD

Presynaptic muscarinic inhibition in bullfrog sympathetic ganglia.

牛蛙交感神经节的突触前毒蕈碱抑制。