摘要
用激光共聚焦技术在急性分离的大鼠背根神经节(DRG)神经元上观察了施加高糖溶液后罗丹明-123(Rhodamine-123)荧光强度的变化,从而推测高血糖对线粒体膜电位的作用及能量代谢的影响。对40个小DRG细胞的观察表明,罗丹明-123荧光强度在细胞的周边最高,而细胞核区的荧光强度最低。当在DRG细胞的培养液(人工脑脊液,ACSF)中滴加30mmol/L的D-葡萄糖溶液后,大部分细胞(8/9)荧光强度迅速降低,在100~400s内,平均降低21.2%±5.4%~22.8%±4.7%。而同体积的ACSF对荧光强度无明显影响(n=7)。滴加葡萄糖后的罗丹明-123荧光强度变化曲线同滴加ACSF后的曲线相比有显著差异(p<0.05)。说明急性高血糖可引起初级传入神经元的能且代谢降低。
Hyperglycemia and decline in the contents of some neuropeptides synthesized by consumption ofenergy in primary afferent neuron have been reported to be associated with the development of diabetic neuropathy. To elucidate the implications of high glucose for nerve dysfunction and the associated changes in enenymetabolism, we measured the Rhodamine fluorescence corresponding to mitochondria Potential by using the advanced laser confer technique in single nerve cell body, which were acutely isolated from newborn rat dorsal rootganglion. An external application of 30 mmol/L glucose caused a transient decrease in the fluorescence of the mitochondria which gradually returned towards the normal level, while the vehicle had no effects on the fluorescence.The finding indicate that the enemy metabolism in the sensory neuron might be impaired by acute hyperplycemia.
出处
《神经科学》
SCIE
CAS
1997年第4期152-156,182,共6页
Chinese Journal of Neuroscience
关键词
背根节神经元
高血糖
激光共聚焦
能量代谢
DRG
hyperglycemia
mitochondria
laser confocal study
energy metabolism