胰岛素样生长因子I可恢复小脑共济失调大鼠模型的运动协调性。
Insulin-like growth factor I restores motor coordination in a rat model of cerebellar ataxia.
作者信息
Fernandez A M, de la Vega A G, Torres-Aleman I
机构信息
Laboratory of Cellular and Molecular Neuroendocrinology, Instituto Cajal, Consejo Superior de Investigaciones Cientificas, Madrid 28002, Spain.
出版信息
Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1253-8. doi: 10.1073/pnas.95.3.1253.
Abstract
We tested the potential of insulin-like growth factor I (IGF-I) to induce functional recovery in an animal model of cerebellar ataxia because this motor impairment is accompanied in humans and rodents by distinct changes in several components of the IGF-I trophic system. Rats rendered ataxic by deafferentation of the cerebellar cortex with 3-acetylpyridine recovered motor function after IGF-I was administered, as determined by behavioral and electrophysiological tests. When treated with IGF-I, inferior olive neurons, the targets of the neurotoxin, were rescued to various degrees (from 92 to 27% of surviving neurons), depending on the time that treatment with IGF-I was initiated. Furthermore, full recovery was obtained regardless of the route by which the trophic factor was administered (intraventricular or subcutaneous) even in rats with severe neuronal loss. These results suggest that human ataxia could be treated with IGF-I by a simple procedure.
摘要
我们测试了胰岛素样生长因子I（IGF-I）在小脑共济失调动物模型中诱导功能恢复的潜力，因为在人类和啮齿动物中，这种运动障碍伴随着IGF-I营养系统多个组成部分的明显变化。通过用3-乙酰吡啶使小脑皮质传入神经脱失而导致共济失调的大鼠，在给予IGF-I后恢复了运动功能，这是通过行为和电生理测试确定的。当用IGF-I治疗时，神经毒素的靶标下橄榄核神经元根据开始用IGF-I治疗的时间不同而有不同程度的挽救（存活神经元的92%至27%）。此外，即使在神经元严重丢失的大鼠中，无论通过何种途径（脑室内或皮下）给予营养因子，都能实现完全恢复。这些结果表明，人类共济失调可以通过简单的程序用IGF-I进行治疗。
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