Spinal Cord Injury-Induced Dysautonomia via Plasticity in Paravertebral Sympathetic Postganglionic

Abstract

Sympathetic postganglionic neurons (SPNs) located in sympathetic ganglia represent the final common sympathetic motor output. Even though SCI produces a profound plasticity in sympathetic autonomic function, the extent that SCI-induced dysautonomia is based on SPN changes within the thoracic paravertebral sympathetic chain is unknown. Given their strategic site in autonomic signaling to body, any plasticity is likely to be of high significance, yet there is a paucity of studies undoubtedly due to their near anatomical inaccessibility. We have solved the accessibility problem with a strategic methodological advance. We will determine the extent to which paravertebral SPNs are a nodal site for vasomotor dysfunction after SCI. We will undertake physiological, pharmacological and optogenetic studies to examine network and cellular plasticity induced by SCI to answer the following two questions: (a) Does SCI lead to plasticity in synaptic interactions between preganglionics, SPNs and primary afferents? (b) Do SPNs become hyper responsive to synaptic inputs after SCI?

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2016
Accession Number
AD1033066

Entities

People

  • Shawn Hochman

Organizations

  • Emory University

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Abstracts
  • Amplitude
  • Autonomic Nervous System
  • Cells
  • Connective Tissue
  • Data Analysis
  • Medical Personnel
  • Membrane Potentials
  • Nervous System
  • Plastic Properties
  • Rodents
  • Spinal Column
  • Spinal Cord
  • Spinal Injuries
  • Spine
  • Students
  • Tissues

Fields of Study

  • Medicine

Readers

  • Cardiovascular Physiology
  • Neuroscience
  • Neurotrauma and Rehabilitation Medicine.