Plasticity in Thoracic Paravertebral Sympathetic Postganglionic Neurons after High Spinal Cord Transection

Area of Science:

• Neuroscience
• Physiology

Background:

• Sympathetic postganglionic neurons (SPNs) control organ function and are modulated by descending brain circuits.
• High thoracic spinal cord injuries (SCIs) disrupt supraspinal control, leading to dysautonomias like hypotension.
• Thoracic SPNs (tSPNs) have functional subpopulations, including Neuropeptide Y-expressing (NPY+) tSPNs, which are putative vasoconstrictors.

Purpose of the Study:

• To investigate whether chronic loss of supraspinal control after SCI induces homeostatic increases in tSPN excitability.
• To characterize changes in intrinsic membrane properties and synaptic function of tSPNs following SCI.

Main Methods:

• Electrophysiological recordings and computational modeling in adult mice (male and female) after high thoracic SCI or sham surgery.
• Analysis of tSPN excitability, intrinsic properties (rheobase, cell resistance, capacitance), dendritic morphology, and synaptic activity (spontaneous excitatory postsynaptic currents).

Main Results:

• tSPN excitability showed a wide range, with a linear relationship between cell resistance and rheobase, obscuring intrinsic plasticity.
• NPY+ tSPNs exhibited reduced dendritic length and capacitance, with increased firing output gain attributed to reduced delayed rectifier currents.
• Spontaneous excitatory synaptic frequency increased significantly after SCI, effectively recruiting spiking activity in tSPNs, particularly in NPY+ tSPNs.

Conclusions:

• Thoracic SPNs, including vasoconstrictors, display compensatory increases in cellular and synaptic excitability following high thoracic SCI.
• These alterations may contribute to mitigating hypotension but could also exacerbate hypertensive responses, such as autonomic dysreflexia.