Cornblath D R, Brown M J
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia.
Exp Neurol. 1988 Feb;99(2):403-11. doi: 10.1016/0014-4886(88)90157-4.
Animals with experimentally induced neuropathies frequently fail to gain weight normally and appear poorly nourished. To determine whether or not malnutrition alone contributes to peripheral nerve dysfunction in these disorders, we subjected healthy 40-day-old rats to three grades of food restriction. After 4 weeks, food-restricted rats weighed 203 +/- 5 (mean +/- SE), 152 +/- 12, and 97 +/- 5 g, respectively, whereas control rats having free access to food weighed 379 +/- 22 g. Posterior tibial nerves of food-deprived rats had smaller endoneurial areas, fewer large-diameter fibers, and shorter internodes than did the nerves of control animals. However, the number of fibers was similar to controls, and there was no evidence of active degeneration or demyelination. Motor and mixed nerve conduction velocities along the same nerves increased with age and did not differ among control and malnourished groups. In growing rats, food deprivation sufficient to impair somatic growth interferes with the maturation of large-caliber myelinated fibers, but does not effect standard electrophysiologic measurements of nerve function.
患有实验性诱发神经病变的动物常常无法正常增重，且显得营养不良。为了确定在这些病症中单纯营养不良是否会导致周围神经功能障碍，我们对40日龄的健康大鼠进行了三个等级的食物限制。4周后，食物受限的大鼠体重分别为203±5（平均值±标准误）、152±12和97±5克，而可自由获取食物的对照大鼠体重为379±22克。与对照动物的神经相比，食物缺乏大鼠的胫后神经神经内膜面积更小、大直径纤维更少且节间更短。然而，纤维数量与对照相似，且没有活跃的变性或脱髓鞘证据。沿着相同神经的运动和混合神经传导速度随年龄增加，且在对照和营养不良组之间没有差异。在生长中的大鼠中，足以损害躯体生长的食物剥夺会干扰大口径有髓纤维的成熟，但不影响神经功能的标准电生理测量。
