Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (21): 1897-1901.doi: 10.4103/1673-5374.145357

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

Lei Cao 1, 2, Xiaohua Bie 1, Su Huo 2, Jubao Du 2, Lin Liu 2, Weiqun Song 2   

  1. 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
  • Received:2014-10-01 Online:2014-11-15 Published:2014-11-15
  • Contact: Weiqun Song, Ph.D., Department of Rehabilitation Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100053, China, songwq66@vip.163.com.
  • Supported by:

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

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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.

Key words: 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