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多巴胺能缺乏导致大鼠视觉诱发电位延迟。

Dopaminergic deficiency causes delayed visual evoked potentials in rats.

作者信息

Onofrj M, Bodis-Wollner I

出版信息

Ann Neurol. 1982 May;11(5):484-90. doi: 10.1002/ana.410110508.

Abstract

Flash and pattern visual evoked potentials (VEPs) to two temporal frequencies of stimulation were studied in nineteen rats. The effect of a tyrosine hydroxylase inhibitor and of a dopamine receptor blocker on the VEP was explored in ten animals. Significant latency change occurred following injection of either drug, while only the hydroxylase inhibitor reduced the VEP amplitude. These changes were not caused by the anesthesia used in these experiments, although the same anesthetics in higher doses did depress VEP amplitudes. When dopamine blockade was followed by administration of apomorphine, a dopamine agonist, VEP delays could be partially reversed. Besides conduction defects of myelinated axons, synaptic malfunction may also cause delays in sensory evoked potentials.

摘要

对19只大鼠进行了针对两种刺激时间频率的闪光和图形视觉诱发电位(VEP)研究。在10只动物中探讨了酪氨酸羟化酶抑制剂和多巴胺受体阻滞剂对VEP的影响。注射任何一种药物后均出现显著的潜伏期变化,而只有羟化酶抑制剂降低了VEP波幅。这些变化并非由这些实验中使用的麻醉引起,尽管更高剂量的相同麻醉剂确实会降低VEP波幅。当多巴胺阻断后给予多巴胺激动剂阿扑吗啡时,VEP延迟可部分逆转。除了有髓轴突的传导缺陷外,突触功能障碍也可能导致感觉诱发电位延迟。

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