Related Experiment Video
Updated: Jun 2, 2026
Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury
Published on: January 20, 2023
Traumatic brain injury impairs synaptic plasticity in hippocampus in rats
Bao-Liang Zhang1, Xin Chen, Tao Tan
1Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
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:
TBI 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.
