首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >EXPERIMENTAL DIABETES IN NEONATAL MICE INDUCES EARLY PERIPHERAL SENSORIMOTOR NEUROPATHY
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EXPERIMENTAL DIABETES IN NEONATAL MICE INDUCES EARLY PERIPHERAL SENSORIMOTOR NEUROPATHY

机译:新生鼠的实验性糖尿病诱发早期外周神经感觉神经病变

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摘要

Animal models of diabetes do not reach the severity of human diabetic neuropathy but relatively mild neuro-physiological deficits and minor morphometric changes. The lack of degenerative neuropathy in diabetic rodent models seems to be a consequence of the shorter length of the axons or the shorter animal life span. Diabetes-induced demyelination needs many weeks or even months before it can be evident by morphometrical analysis. In mice myelination of the peripheral nervous system starts at the prenatal period and it is complete several days after birth. Here we induced experimental diabetes to neonatal mice and we evaluated its effect on the peripheral nerve 4 and 8 weeks after diabetes induction. Neurophysiological values showed a decline in sensory nerve conduction velocity at both time-points. Morphometrical analysis of the tibial nerve demonstrated a decrease in the number of myelinated fibers, fiber size and myelin thickness at both time-points studied. Moreover, aldose reductase and poly(ADP-ribose) polymerase activities were increased even if the amount of the enzyme was not affected. Thus, type 1 diabetes in newborn mice induces early peripheral neuropathy and may be a good model to assay pharmacological or gene therapy strategies to treat diabetic neuropathy.
机译:糖尿病的动物模型没有达到人类糖尿病性神经病的严重程度,但是相对轻度的神经生理缺陷和较小的形态变化。糖尿病啮齿动物模型中缺乏变性神经病似乎是轴突长度较短或动物寿命较短的结果。糖尿病引起的脱髓鞘需要数周甚至数月的时间才能通过形态计量学分析证实。在小鼠中,周围神经系统的髓鞘形成始于产前期,并且在出生后几天就完成了。在这里,我们向新生小鼠诱导了实验性糖尿病,并在诱导糖尿病后4和8周评估了其对周围神经的作用。神经生理学值在两个时间点均显示感觉神经传导速度下降。胫神经的形态计量学分析表明,在所研究的两个时间点,髓鞘纤维的数量,纤维大小和髓鞘厚度的减少。而且,醛糖还原酶和聚(ADP-核糖)聚合酶活性增加,即使该酶的量不受影响。因此,新生小鼠中的1型糖尿病会诱发早期周围神经病变,并且可能是测定用于治疗糖尿病性神经病变的药理或基因治疗策略的良好模型。

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