Copper as a trace metal is involved in several neurodegenerative illnesses, such as Menkes, Wilson's, Alzheimer's, amyotrophic lateral sclerosis (ALS), and Creutzfeldt-Jakob. Electrophysiological evidence indicates that acute perfusion of copper can inhibit long-term synaptic potentiation in hippocampal slices. The objective of this work is to determine whether Cu perfusion can perturb synaptic transmission in hippocampal slices derived from pilocarpine treated epileptic rats. Field potential (FP) recordings of the CA1 neurons of rats with chronic epilepsy showed voltage and response duration decrease following copper sulfate perfusion. However, voltage and response duration were higher after removing copper by washing. The discharge frequency of the CA1 neurons of hippocampal slices from non-epileptic control rats was increased after acute perfusion of 10 μM of pilocarpine. This increase was blocked by administering copper sulphate 10 μM. Krebs-Ringer solution washing re-established the discharges, with a higher frequency than that provoked by pilocarpine perfusion. We discuss the blocking effect of copper and the synaptic hyper-excitability generated by its removal.

中文翻译：

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铜的施用降低了癫痫大鼠CA1海马切片中神经元的过度兴奋性。

铜作为痕量金属参与多种神经退行性疾病，例如Menkes，Wilson病，阿尔茨海默氏病，肌萎缩性侧索硬化症（ALS）和Creutzfeldt-Jakob。电生理证据表明，铜的急性灌注可抑制海马切片中的长期突触增强。这项工作的目的是确定铜灌注是否可以干扰源自毛果芸香碱治疗的癫痫大鼠的海马切片中的突触传递。慢性癫痫大鼠的CA1神经元的场电位（FP）记录显示，硫酸铜灌注后电压和响应时间降低。然而，通过洗涤除去铜后，电压和响应持续时间较高。急性灌注10μM毛果芸香碱后，非癫痫对照大鼠海马切片CA1神经元的放电频率增加。通过添加10μM硫酸铜可阻止这种增加。克雷布斯-林格（Krebs-Ringer）溶液洗涤重新建立了放电，其频率高于毛果芸香碱灌注引起的放电频率。我们讨论了铜的阻滞作用和去除铜所产生的突触超兴奋性。