| Objective:To investigate the changes of the outward delayed rectifier potassium currents in motoneurons of the spinal ventral horn in neonatal rats subjected to transection and Tetramethypyrazine(TMP)administration,and to explore the therapy mechanism of TMP on the spinal cord injury.Methods:Neonatal Sprague Dawley(SD)rats were randomly divided into two groups:normal group(n=12)and transection group(T10level,n=10),and every group was administrated of TMP(8mM)respectively.The spinal cord of L3-L5 segments were harvested to make the slices,then incubated at 36℃for 1h.The outward delayed rectifier potassium currents of every group were recorded at the same holding voltage by the whole-cell of patch clamp technique.Results:The outward delayed rectifier potassium currents were successfully recorded in normal and transected rats.The outward delayed rectifier potassium currents density increased following transection,while there is no significant difference.TMP addition obviously attenuate the outward delayed rectifier potassium currents density in both normal and transected animals.TMP addition also attenuate the amplitude of the outward delayed rectifier potassium currents in transected animals(P＜0.01).A significant difference in inhibition ratio was found in TMP groups.The effect of TMP can be deleted following the wash of ACSF.Conclusion:There were outward delayed rectifier potassium currents in both normal and transected rats.TMP addition can inhibit the outward delayed rectifier potassium currents density and amplitude in motoneurons of the spinal ventral horn in normal and transection rats,and the effect of TMP on transection rats was obviously. Based on increase of outward delayed rectifier potassium currents is linked to cell apoptosis,the present findings indicated that effect of TMP for neuroprotection on the injured spinal cord motoneurons may be associated to the changes of outward delayed rectifier potassium currents.
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