Relationship between learning and memory deficits and Arp2 expression in the hippocampus in rats with traumatic brain...

To investigate the learning and memory impairments at acute phase after mild traumatic brain injury (TBI) in Sprague-Dawley rats and its relationship with the expression of Arp2.

Hundred adult male Sprague-Dawley rats were randomly assigned into a TBI group or a control group. TBI was produced by using an impact acceleration model. Learning and memory function was assessed using Morris Water Maze test after different injury intervals, and synaptic function was investigated after TBI treatment by using field excitatory postsynaptic and long-term potentials. Western blot, immunochemistry, and polymerase chain reaction (PCR) were used to detect the mRNA and protein expression of actin-related protein 2 (Arp2) after injury, whereas Nissl staining and DNA ladder assays were performed to detect neuron apoptosis.

Using water maze measurement, the authors found escape latency to be significantly higher in the TBI group compared with the control group, and at 7 days postinjury, the difference almost reached up to 30 seconds. Field excitatory postsynaptic potential measurement further found that the long-term potential decreased by nearly 20% in the TBI group compared with the control group, which meant the synaptic excitatory function was downregulated in the TBI group. Further, no significant neuron apoptosis could be detected in the TBI group by Nissl staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and DNA ladder assays. At last, we found that after TBI treatment, the Arp2 mRNA and protein levels were decreased in a time-dependent manner and reached 29.3% and 45.7% of control at 7 days postinjury, separately, and the decrease of mRNA of Arp2 was correlated with delayed escape latency.

This study demonstrated that impairments of learning and memory function in the acute phase after mild TBI may be induced by a reduction in Arp2 expression.