Abstract:

BACKGROUND: Peripheral nerve injuries can cause Ca²⁺ channel opening in the cell membrane and the extracellular Ca²⁺ internal flow, thereby resulting in intracellular calcium overload.
OBJECTIVE: To observe free Ca²⁺ concentration changes in the spinal cord anterior horn motor neurons after brachial plexus root rupture injury.
METHODS: Eighty-four healthy adult male Wister rats were randomly divided into three groups: sham operation group, control group and experimental group. Rats in the sham operation group were only subjected to expose the brachial plexus nerve without rupture. Rats in the control group had not treatment after brachial plexus nerve injury and those in the experimental group were intraperitoneally injected with 4 mg/(kg·d) verapamil. After the nerve was cut for 12 hours, 24 hours, 48 hours, 72 hours, 1 week, 2 weeks, and 4 weeks, four samples was collected from each group.
RESULTS AND CONCLUSION: At the beginning of peripheral nerve injury, Ca²⁺ concentration in the spinal cord anterior horn motor neurons of the control and experimental groups was increased and reached a peak after 48 hours, but subsequently was decreased gradually. After 1 week, Ca²⁺ concentration of the experimental group basically returned to a normal level, but was still higher than that of the sham operation group. These results suggest that after brachial plexus root rupture injury, the L-type Ca²⁺channel on the nerve cell membrane is open, and Ca²⁺ internal flow enters into the cells, which leads to the increase in intracellular free Ca²⁺concentration. Moreover, L-type Ca²⁺channel can be blocked by verapamil, to decrease the Ca²⁺ internal flow and the number of apoptotic motor neurons.