Associated norepinephrine loss following calcium-induced spinal paralysis

Document Type

Article

Department

Brain and Mind Institute

Abstract

A 10% calcium chloride solution or normal physiological saline was instilled onto the intact dorsal surface of the spinal cord via a specially constructed catheter-canopy system fixed above the T9 level in conscious rats. Within 5 min after calcium instillation rats developed flaccid paralysis of the lower limbs with sensory loss. Sensory loss was accompanied by abnormal or negative evoked potentials. Rats instilled with physiological or 10% sodium chloride remained normal. Rats were sacrificed at 1, 16 and 48 h post-calcium exposure and following full functional recovery from paralysis. Spinal cords were removed for histologic and high-performance liquid chromatography (HPLC) analysis. Histologic examination for catecholamines using SPG histofluorescence showed loss of catecholamine-containing varicosities in gray matter below calcium exposure which returned to normal levels upon sensorimotor recovery of hindlimbs about 14 days pce. Light microscopic examination of vascular permeability and general morphology of cord tissue axons and neurons remained normal in calcium and saline instilled rats. HPLC analysis of spinal cord below calcium exposure, also showed norepinephrine (NE) and 3-methoxy-4-hydroxyphenylglycol (MHPG) tissue level reductions which returned to normal upon sensorimotor recovery of paralysis about 2 weeks later. No significant changes were noted in dopamine or serotonin levels in any group. Our findings suggest an impairment of ascending and descending tract transmitter transport, specifically reflected in the noradrenergic bulbospinal pathway. The results implicate a neurofilament-microtubule disassembly in axonal cytoskeleton triggered by the sudden calcium influx.

Comments

This work was published before the author joined Aga Khan University.

Publication (Name of Journal)

Brain Research

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