Structural neuroplasticity following T5 spinal cord transection: increased cardiac sympathetic innervation density and SPN arborization.
When the spinal cord is injured at or below thoracic level 5 (T5), cardiovascular control is markedly unbalanced as the heart and blood vessels innervated by upper thoracic segments remain under brain stem control, whereas the vasculature of the lower body is affected by unregulated spinal reflexes. Importantly, the regulation of heart rate and cardiac function is abnormal after spinal cord injury (SCI) at T5 because sympathetic outflow to the heart is increased. An increase in tonic sympathetic outflow may be attributable to multiple mechanisms, such as increases in cardiac sympathetic innervation density, altered morphology of stellate ganglia neurons, and/or structural neuroplasticity of cardiac sympathetic preganglionic neurons (SPNs). Furthermore, these neuroplastic changes associated with SCI may be mediated by nerve growth factor (NGF). NGF is a neurotrophin that supports the survival and differentiation of sympathetic neurons and enhances target innervation. Therefore, we tested the hypothesis that T5 spinal cord transection (T5X) is associated with an increased left ventricular (LV) NGF content, LV sympathetic innervation density, and cardiac SPN arborization. In intact and paraplegic (9 wk posttransection) rats, LV NGF content (ELISA), LV sympathetic innervation density (tyrosine hydroxylase immunohistochemistry), and cardiac SPN arborization (cholera toxin B immunohistochemistry and Sholl Analysis) were determined. Paraplegia, compared with intact, significantly increased LV NGF content, LV sympathetic innervation density, and cardiac SPN arborization. Thus, altered autonomic behavior following SCI is associated with structural neuroplastic modifications.
Lujan
Heidi L
HL
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
Palani
Gurunanthan
G
DiCarlo
Stephen E
SE
D000818:Animals; D001339:Autonomic Fibers, Preganglionic / Q000502:physiology*; D002772:Cholera Toxin / Q000494:pharmacology; D004396:Coloring Agents; D003712:Dendrites / Q000502:physiology / Q000648:ultrastructure; D004797:Enzyme-Linked Immunosorbent Assay; D006321:Heart / Q000294:innervation*; D007150:Immunohistochemistry; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D020932:Nerve Growth Factor / Q000378:metabolism; D009434:Neural Pathways / Q000473:pathology / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*; D013233:Stellate Ganglion / Q000473:pathology / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D016277:Ventricular Function, Left / Q000502:physiology
D004396:Coloring Agents; D002772:Cholera Toxin; D020932:Nerve Growth Factor; D014446:Tyrosine 3-Monooxygenase