O'Dell B L, Conley-Harrison J, Besch-Williford C, Browning J D, O'Brien D
Department of Biochemistry, University of Missouri, Columbia 65211.
FASEB J. 1990 Aug;4(11):2919-22. doi: 10.1096/fasebj.4.11.2165949.
Guinea pigs fed a diet low in zinc develop clinical signs of apparent neurological origin. The signs include abnormal posture and locomotion as well as hypersensitivity to touch. In this study, electrophysiological and biochemical measurements were made on sciatic nerves from zinc-deficient and repleted animals as well as on controls fed either ad libitum or restricted to maintain weight comparable to those consuming the deficient diet. Both in vivo and in vitro measurements showed decreased motor nerve conduction velocity (NCV) in nerves of deficient animals. A longitudinal study showed excellent correlation of NCV and severity of clinical signs. Nerves from zinc-deficient guinea pigs had decreased Na,K-ATPase activity, but the number of sodium channels, as determined by saxitoxin binding, was not affected. It was concluded that the clinical signs of neuropathy in zinc deficiency are associated with impaired NCV and decreased Na,K-ATPase activity of peripheral nerves. The zinc-deficient guinea pig provides a useful model to study the biochemical defect in a peripheral neuropathy.
喂食低锌饮食的豚鼠会出现明显源于神经学的临床症状。这些症状包括异常姿势和运动以及对触摸过敏。在本研究中，对缺锌和补锌动物的坐骨神经以及自由采食或限制采食以维持体重与食用缺锌饮食的动物相当的对照组动物的坐骨神经进行了电生理和生化测量。体内和体外测量均显示缺锌动物神经中的运动神经传导速度（NCV）降低。一项纵向研究表明NCV与临床症状严重程度具有良好的相关性。缺锌豚鼠的神经中钠钾ATP酶活性降低，但由石房蛤毒素结合测定的钠通道数量未受影响。得出的结论是，锌缺乏时神经病变的临床症状与外周神经NCV受损和钠钾ATP酶活性降低有关。缺锌豚鼠为研究周围神经病变中的生化缺陷提供了一个有用的模型。
