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 hyperresponsive to synaptic inputs after SCI?