Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury  

作　　者：Lei Cao Xiaohua Bie Su Huo Jubao Du Lin Liu Weiqun Song 

机构地区：[1]Department of Functional Neurosurgery,Xi’an Red Cross Hospital [2]Department of Rehabilitation Medicine,Xuanwu Hospital,Capital Medical University

出　　处：《Neural Regeneration Research》2014年第21期1897-1901,共5页中国神经再生研究（英文版）

基　　金：supported by the National Natural Science Foundation of China,No.81201984;the Scientific Research Project of Shaanxi Provincial Health Department in China,No.2010E03;the Yulin Municipal Science and Technology Research and Development Project,No.Sf12-06

摘　　要：The activity of the Schaffer collaterals of hippocampal CA3 neurons and hippocampal CA1 neurons has been shown to increase after lfuid percussion injury. Diazepam can inhibit the hy-perexcitability of rat hippocampal neurons after injury, but the mechanism by which it affects excitatory synaptic transmission remains poorly understood. Our results showed that diazepam treatment signiifcantly increased the slope of input-output curves in rat neurons after lfuid per-cussion injury. Diazepam signiifcantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 μmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus. Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release. These data suggest that diazepam could decrease the lfuid per-cussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.The activity of the Schaffer collaterals of hippocampal CA3 neurons and hippocampal CA1 neurons has been shown to increase after lfuid percussion injury. Diazepam can inhibit the hy-perexcitability of rat hippocampal neurons after injury, but the mechanism by which it affects excitatory synaptic transmission remains poorly understood. Our results showed that diazepam treatment signiifcantly increased the slope of input-output curves in rat neurons after lfuid per-cussion injury. Diazepam signiifcantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 μmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus. Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release. These data suggest that diazepam could decrease the lfuid per-cussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.

关 键 词：nerve regeneration traumatic brain injury fluid percussion injury excitatory synaptic transmission hippocampal CA1 pyramidal neurons paired-pulse facilitation miniature excitatory postsynaptic potential gamma-aminobutyric acid post-traumatic hyperactivity intracellular recording NSFC grant neural regeneration 

分 类 号：R651.15[医药卫生—外科学]