Sabel B A, Dunbar G L, Stein D G
J Neurosci Res. 1984;12(2-3):429-43. doi: 10.1002/jnr.490120227.
Injections of GM1-gangliosides (30 mg/kg, i.p.) in adult rats were shown to reduce behavioral deficits after brain lesions. This was observed (1) after bilateral electrolytic lesions of the caudate nucleus in a learning task involving negative reinforcement; (2) following aspiration lesions of the mediofrontal cortex in a learning task involving positive reinforcement; and (3) when rotational behavior was assessed after amphetamine or apomorphine injections in animals with partial hemitransections of the nigro-striato-nigral fibers. A detailed anatomical analysis of the latter study, using a retrograde tract-tracing dye wheat germ agglutinin-horseradish peroxidase (WGA-HRP), provided evidence for ganglioside-stimulated, neuronal reorganization of connections to the caudate nucleus. Our findings support the notion that gangliosides reduce behavioral deficits following brain injury by preventing secondary neuronal degeneration and/or enhancing structural reorganization of remaining afferents, rather than by influencing denervation supersensitivity.
在成年大鼠中腹腔注射神经节苷脂GM1（30毫克/千克）可减少脑损伤后的行为缺陷。这一现象在以下情况中被观察到：（1）在涉及负强化的学习任务中，尾状核双侧电解损伤后；（2）在涉及正强化的学习任务中，额中回皮质抽吸损伤后；（3）在黑质-纹状体-黑质纤维部分横断的动物中，注射苯丙胺或阿扑吗啡后评估旋转行为时。在后者的研究中，使用逆行示踪染料小麦胚凝集素-辣根过氧化物酶（WGA-HRP）进行详细的解剖学分析，为神经节苷脂刺激的、与尾状核连接的神经元重组提供了证据。我们的研究结果支持这样的观点，即神经节苷脂通过防止继发性神经元变性和/或增强剩余传入神经的结构重组来减少脑损伤后的行为缺陷，而不是通过影响去神经超敏反应。
