Abstract
Spinal cord injury is an extremely severe condition with no available effective therapies. We examined the effect of melatonin on traumatic compression of the spinal cord. Sixty male adult Wistar rats were divided into three groups: sham-operated animals and animals with 35 and 50% spinal cord compression with a polycarbonate rod spacer. Each group was divided into two subgroups, each receiving an injection of vehicle or melatonin (2.5 mg/kg, intraperitoneal) 5 min prior to and 1, 2, 3, and 4 h after injury. Functional recovery was monitored weekly by the open-field test, the Basso, Beattie and Bresnahan locomotor scale and the inclined plane test. Histological changes of the spinal cord were examined 35 days after injury. Motor scores were progressively lower as spacer size increased according to the motor scale and inclined plane test evaluation at all times of assessment. The results of the two tests were correlated. The open-field test presented similar results with a less pronounced difference between the 35 and 50% compression groups. The injured groups presented functional recovery that was more evident in the first and second weeks. Animals receiving melatonin treatment presented more pronounced functional recovery than vehicle-treated animals as measured by the motor scale or inclined plane. NADPH-d histochemistry revealed integrity of the spinal cord thoracic segment in sham-operated animals and confirmed the severity of the lesion after spinal cord narrowing. The results obtained after experimental compression of the spinal cord support the hypothesis that melatonin may be considered for use in clinical practice because of its protective effect on the secondary wave of neuronal death following the primary wave after spinal cord injury.
Highlights
Spinal cord injury (SCI) results in the loss of function below the lesion
The results reported here support the benefit of exogenous melatonin as a therapeutic intervention for spinal cord injury induced by compression
In the 50%-V animals, an additional decrease was detected at days 1, 7, 14, and 28, this decrease was more pronounced in the 50%-V group than in the 35%-V group only on the first day (F2,19 variation from 6.13 to 29.02, P, 0.01)
Summary
Spinal cord injury (SCI) results in the loss of function below the lesion. The compression of the spinal cord that follows vertebral displacement and edema is considered to be a very frequent cause of traumatic spinal cord lesion. Secondary injury following the primary impact includes a number of biochemical and cellular alterations, localized edema, hemorrhage, thrombosis, vasospasm, and loss of vasculature autoregulation [1]. Primary traumatic mechanical injury to the spinal cord causes the death of a number of neurons that cannot be recovered or regenerated. Some neurons continue to die for hours after traumatic SCI [2,3]. This secondary neuronal death may be caused by substances released from cells in response to the primary injury. The initial procedures are thought to be decisive for the evolution of the events that ensue during the evolution of the injury [1]
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