Abstract
Spinal cord ischemia and reperfusion (SCIR) injury is the major cause of a wide range of complications, including neural degeneration and devastating paraplegia. Decrease of inhibitory neurotransmitters and increase of excitory neurotransmitters are the major cause for the excitotoxicity of neurons. However, no study has reported the temporal loss of motor neuron in the ventral horn of spinal cord area following SCIR-induced spastic paralysis, not even the mechanism under it. In the present study, we found that the rabbits were mainly spastic paralyzed after spinal cord ischemia-reperfusion injury. And the ischemia 60 min group is the optimal treating condition, because of the higher rate of spastic paralysis and lower mortality. Motor neurons in the ventral horn of spinal cord were significant degeneration at 3 h following spastic paralysis and only 12.5% motor neurons were observed at 72 h post-operation, compared with control group. ELISA results indicated that Glycine and GABA were both downregulated following spastic paralysis. But Glycine immediately decreased at 10 min post-operation and lasted for the whole process (at least 72 h). Meanwhile GABA only significantly decreased at 72 h. Furthermore, Glutamic expression was significant upregulation at 3 hours post-operation, and the upregulation back to the base level at 72 h post-operation. Glutamic receptor-(NR1) and Glycine α1 receptor upregulated accordingly, whereas GABBR2 didn't upregulate significantly until at 72 h post-operation. Abundant extracellular Ca2+ influxed into cytoplasm in neurons following spastic paralysis. The type of paraplegia is mainly spastic paraplegia after SCIR (ischemia 60 min treatment). Following spastic paraplegia, motor neuron in the ventral horn of spinal cord area was significant degeneration at early stage and last for the whole process. It may contribute to the decrease of Glycine at early stage and followed exitotoxicity, which caused intracellular calcium overload to make neurons dead. It would lay the foundation for better understanding the motor neuron degeneration and mechanism following spastic paralysis. And it would supply a novel and effective target for spastic paralysis prevention and therapy.