Plasticity of sympathetic post‐ganglionic neuron after spinal cord injury

Abstract

Autonomic dysreflexia (AD) is a hypertensive crisis seen in high‐thoracic spinal cord injured (ht‐SCI) patients normally triggered by noxious stimuli below the injury level. Previous animal research on mechanisms underlying AD have mostly focused on neural plasticity within the injured spinal cord. No studies have assessed whether there is also plasticity in the sympathetic post‐ganglionic neurons (SPNs) ‐ the final neural element responsible for vasoconstriction.Thoracic sympathetic post‐ganglionic neurons (tSPNs) are located in paravertebral ganglia and provide the dominant sympathetic control of blood pressure. Their cellular properties are understudied. The few previous ex vivo studies used sharp electrodes that likely leads to significant impalement injury‐induced changes [1, 2]. We undertook whole‐cell patch clamp recordings in an adult mouse tSPN ex vivo preparation. Compared to earlier reports using sharp electrodes, we observed an order of magnitude greater passive membrane properties (cell resistance and membrane time constant) and repetitive rather than phasic firing properties. Together these observations support much greater excitability and integrative actions of tSPNs than previously assumed.Using the same methodology we then studied whether these neurons undergo plastic changes after high‐thoracic (T2) spinal cord transection (ht‐SCI), an animal model of AD. Recordings were obtained from T3‐T9 tSPNs at 3 weeks and 6 weeks post injury. Preliminary data suggest that early after injury (3 weeks), tSPNs are hypo‐active compared to normal animal, including more hyperpolarized resting membrane potential and higher rheobase and threshold voltage. At 6 weeks post‐SCI, tSPN passive membrane properties are similar to control mice. However, several neurons show spontaneously unstable membrane potential (55% of recorded neurons), which is rarely seen in control. Evidences that tSPNs may become more excitable include lower rheobase and threshold voltage values on average and an increased incidence of nifedipine sensitive persistent inward currents (PIC; 69% of recorded neurons after SCI has PIC comparing to 22% in control). Also, tSPNs appear to receive more frequent spontaneous cholinergic synaptic input after SCI.Support or Funding InformationThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.