Histological Characterization of Descending Serotonergic Input to Sympathetic Preganglionic Neurons After Spinal Cord Injury
Abstract
Spinal cord injury (SCI) disrupts descending pathways that regulate sympathetic preganglionic neurons (SPNs), which serve as the final central output controlling sympathetic baroreflex regulation of blood pressure. Loss of supraspinal input after SCI contributes to cardiovascular instability, including orthostatic hypotension which leads to dizziness upon change in position and can lead to inability to participate in physical therapy exercises. The specific neural pathways involved and their organization within spinal sympathetic regions remain incompletely understood. Bulbospinal serotonergic (5-hydroxytryptamine, 5-HT) projections are known modulators of spinal autonomic circuits, but their structural organization in the early post-injury period has not been fully characterized. The objective of this study is to examine descending serotonergic input to SPNs caudal to injury to identify pathway-level changes that may contribute to altered autonomic regulation. We hypothesize that SCI will reduce serotonergic input within sympathetic regions below the lesion and that diminished descending modulation may be associated with reduced activation of sympathetic circuits. Adult rats received a left T7 spinal hemisection and were studied one week post-injury. SPNs are identified in thoracic spinal cord sections using immunohistochemical labeling for choline acetyltransferase (ChAT), and serotonergic input is visualized using 5-HT immunolabeling. Sections are imaged with fluorescence microscopy and three-dimensional deconvolution within standardized regions of interest in the intermediolateral cell column. Planned analyses include quantification of 5-HT immunoreactive fiber density within sympathetic regions and comparisons between sides relative to the lesion. Lesion extent is verified histologically in each subject, and measurements caudal to injury are normalized to rostral segments within animals to control for staining variability. By characterizing how specific descending inputs to SPNs are organized after SCI, this work aims to clarify which neural pathways may contribute to altered autonomic cardiovascular regulation and to provide an anatomical framework for understanding mechanisms underlying early autonomic dysfunction following spinal cord injury.
Start Time
15-4-2026 1:30 PM
End Time
15-4-2026 2:30 PM
Room Number
219
Presentation Type
Oral Presentation
Presentation Subtype
UG Orals
Presentation Category
Health
Student Type
Undergraduate
Faculty Mentor
Matthew Zahner
Histological Characterization of Descending Serotonergic Input to Sympathetic Preganglionic Neurons After Spinal Cord Injury
219
Spinal cord injury (SCI) disrupts descending pathways that regulate sympathetic preganglionic neurons (SPNs), which serve as the final central output controlling sympathetic baroreflex regulation of blood pressure. Loss of supraspinal input after SCI contributes to cardiovascular instability, including orthostatic hypotension which leads to dizziness upon change in position and can lead to inability to participate in physical therapy exercises. The specific neural pathways involved and their organization within spinal sympathetic regions remain incompletely understood. Bulbospinal serotonergic (5-hydroxytryptamine, 5-HT) projections are known modulators of spinal autonomic circuits, but their structural organization in the early post-injury period has not been fully characterized. The objective of this study is to examine descending serotonergic input to SPNs caudal to injury to identify pathway-level changes that may contribute to altered autonomic regulation. We hypothesize that SCI will reduce serotonergic input within sympathetic regions below the lesion and that diminished descending modulation may be associated with reduced activation of sympathetic circuits. Adult rats received a left T7 spinal hemisection and were studied one week post-injury. SPNs are identified in thoracic spinal cord sections using immunohistochemical labeling for choline acetyltransferase (ChAT), and serotonergic input is visualized using 5-HT immunolabeling. Sections are imaged with fluorescence microscopy and three-dimensional deconvolution within standardized regions of interest in the intermediolateral cell column. Planned analyses include quantification of 5-HT immunoreactive fiber density within sympathetic regions and comparisons between sides relative to the lesion. Lesion extent is verified histologically in each subject, and measurements caudal to injury are normalized to rostral segments within animals to control for staining variability. By characterizing how specific descending inputs to SPNs are organized after SCI, this work aims to clarify which neural pathways may contribute to altered autonomic cardiovascular regulation and to provide an anatomical framework for understanding mechanisms underlying early autonomic dysfunction following spinal cord injury.
