Research on the changes in balance motion behavior and learning, as well as memory abilities of rats with multiple cerebral concussion-induced chronic traumatic encephalopathy and the underlying mechanism

Abstract

To study the effects of multiple cerebral concussion (MCC)-induced chronic traumatic encephalopathy on balance motion behavior learning and memory abilities of rats and its possible mechanism. 4MCC rat models were established by means of striking the head (4MCC group, n=15), while normal Sprague-Dawley (SD) rats were used as controls (C group, n=15). At 2 weeks after injury, balance beam (BB) test, beam walking (BW) test and Morris water maze (MWM) test were performed, respectively. The metabolites in brain tissues of rats, the number of glial fibrillary acidic protein (GFAP)-positive cells and apoptotic cells in brain slices of rats, and the expression levels of phosphorylated tau (p-tau) and Aβ1-40 proteins were detected. The score of rats in 4MCC group was significantly lower than that in C group (p<0.01). The escape latencies of rats in 4MCC group on the 4th-7th days during training and the time reaching the platform were significantly longer (p<0.05), but the residence time in the target quadrant was obviously shorter (p<0.01). Naphthalene acetic acid (NAA) and creatinine (Cr) values in septal coronal section in 4MCC group were significantly lower, but choline (Cho) and myo-inositol (MI) values were obviously higher (p<0.01). The number of GFAP-positive cells in the hippocampal and septal areas in 4MCC group were significantly larger (p<0.01). In the hippocampal and septal areas of 4MCC group, the number of apoptotic cells was obviously larger (p<0.01), and the expression levels of p-tau and Aβ1-40 proteins were significantly higher (p<0.01). Thus, MCC-induced chronic traumatic encephalopathy can increase the expressions of p-tau and Aβ1-40 proteins in the hippocampal and septal areas, leading to damage of hippocampal and septal neurons and increasing the number of astrocytes in the hippocampal and septal areas, ultimately damaging the balance motion behavior and learning, as well as memory abilities of rats.

Traumatic brain injury and the pathways to cerebral tau accumulation

“…It is important to note the differences in subjects, injury model, and number of injuries and intervals between these studies. Those studies examining a single acute (< 30 days) timepoint also showed variability; a weight drop injury showed no tau histology changes in brainstem at 1d ( 116 ), a frontal pendulum rmTBI showed decreased pTau at 14 days ( 117 ), and a weight drop in mice showed increased p-tau at 30 days ( 118 ). The remaining studies examining a single chronic time point showed some increase in p-tau but they were not robust ( 119–121 ), and one study showed p-tau even decreased compared to 1 day ( 122 ).…”