周围神经损伤后脊髓前角运动神经元内游离Ca2+的浓度

背景：神经损伤后可引起细胞膜上Ca²⁺通道的开放，使细胞外Ca²⁺内流，造成细胞内的钙超载。 目的：观察臂丛神经根切断伤后相应脊髓前角运动神经元内游离Ca²⁺浓度的变化。 方法：健康成年雄性Wistar大鼠84只，分为3组：假手术组暴露臂丛神经不切断；对照组臂丛神经切断伤后不做其他处理；实验组臂丛神经切断伤后，给予腹腔注射Ca2+阻带剂维拉帕米4 mg/(kg?d)。于切断伤后12 h，24 h，48 h，72 h，1周，2周，4周每组随机以4只取材。 结果与结论：周围神经损伤开始，对照组及实验组大鼠损伤侧脊髓前角运动神经元细胞内Ca²⁺浓度开始升高，至伤后48 h达高峰，此后逐渐下降，伤后1周，实验组已基本回至正常水平，但仍较假手术组高。说明神经损伤后相应神经元细胞膜上L型Ca²⁺通道开放，Ca2+内流进入细胞内，导致神经细胞内游离Ca²⁺浓度增加，L型Ca²⁺通道可以被维拉帕米阻断，减少神经损伤后的Ca²⁺内流，减少神经细胞凋亡的数量。

Ca2+ concentration changes in the spinal motoneurons after brachial plexus root rupture injury

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.