摘要
Background Traumatic brain injury （TBI） often causes cognitive deficits and remote symptomatic epilepsy. Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBI may impair the cellular circuit in the hippocampus.Methods Forty male Wistar rats were randomized into control （n=-20） and TBI groups （n=20）. Long-term potentiation, extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.Results TBI resulted in a significantly increased excitability in the dentate gyrus （DG）, but a significantly decreased excitability in the cornu ammonis 1 （CA1） area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area. Conclusions TBl leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.
Background Traumatic brain injury （TBI） often causes cognitive deficits and remote symptomatic epilepsy. Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBI may impair the cellular circuit in the hippocampus.Methods Forty male Wistar rats were randomized into control （n=-20） and TBI groups （n=20）. Long-term potentiation, extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.Results TBI resulted in a significantly increased excitability in the dentate gyrus （DG）, but a significantly decreased excitability in the cornu ammonis 1 （CA1） area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area. Conclusions TBl leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.
基金
This work was supported by grants from the National ＂973 Projects＂ of China （No. 2005CB522605）, Tianjin Science and Technology Development Plan （No. 05YFGDSF02500） and Tianjin Natural Science Foundation （No. 033611511）. No competing financial interests exist.
