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SPINAL MECHANISMS CONTROLLING MOTONEURON EXCITABILITY

控制运动神经元兴奋性的脊髓机制

基本信息

批准号：
2703046
负责人：
FLOYD J. THOMPSON
金额：
$ 12万
依托单位：
UNIVERSITY OF FLORIDA
依托单位国家：
美国
项目类别：
财政年份：
1995
资助国家：
美国
起止时间：
1995-05-01 至 2000-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/2703046
关键词：
GABA receptor disease /disorder model laboratory rat membrane potentials motor neurons neural inhibition neural plasticity spastic paralysis spinal cord injury spinal reflex

项目摘要

DESCRIPTION (Taken from applicant's abstract) These investigators have recently observed a robust change in rate-depression (a progressive decline in the monosynaptic reflex at low stimulation frequencies) in rats following the type of spinal cord injury which typically induces spasticity in humans. This experimental model provides an opportunity to determine some essential features of the neurosubstrate and cellular mechanisms of rate-depression. Preliminary data show that rate-depression is significantly reduced by blockade of GABAb receptors by intrathecal administration of a specific GABAb antagonist. However, both spinal and supraspinal sites could have accounted for these observations. Experiments in Specific Aim 1 are proposed using intraspinal microinjection of GABAb agonists and antagonists to identify specific sites within the spinal cord which alter rate-depression. These studies will more specifically define the segmental neural substrate and cellular mechanisms of action of rate-depression. Further evidence indicates that rate- depression can be significantly influenced by microstimulation of cell clusters in the brainstem which are associated with the densest spinal projection of serotonergic fibers. Therefore, insights into the descending control of rate-depression will be sought using microstimulation to identify brainstem neuron and fiber clusters which significantly alter the expression of rate-depression. These studies will increase understanding of the descending control of reflex excitability as well as account for changes which occur following spinal cord injury. Experiments in Specific Aim 2 will determine how specific changes in reflex excitability may correlate to the experimental manifestation of spastic hyperreflexia. These experiments will correlate the time course and magnitude of alterations in the dynamic stretch reflexes of lower leg calf muscles to specific changes in spinal reflex excitability following midthoracic spinal hemisection. In addition the specific role of GABAb receptors in the maintenance of normal muscle tone, as well as the development and persistence of spastic hypertonia of calf muscle dynamic stretch reflexes will be determined. In summary, the proposed experiments will increase our understanding of the mechanism and organization of a fundamental process which regulates motoneuron excitability and how changes in the mechanism may contribute to the development of spastic hypertonia.

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