Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury |
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Authors: | Lei Cao ;Xiaohua Bie ;Su Huo ;Jubao Du ;Lin Liu ;Weiqun Song |
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Institution: | [1]Department of Functional Neurosurgery, Xi'an Red Cross Hospital, Xi'an, Shaanxi Province, China; [2]Department of Rehabilitation Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China |
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Abstract: | The activity of the Schaffer collaterals of hippocampal CA3 neurons and hippocampal CA1 neurons has been shown to increase after fluid percussion injury. Diazepam can inhibit the hyperexcitability 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 significantly increased the slope of input-output curves in rat neurons after fluid percussion injury. Diazepam significantly 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 fluid percussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area. |
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Keywords: | 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 |
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