Abstract

Moderate traumatic brain injury (TBI) in children often happen when there’s a sudden blow to the frontal bone, end with long unconscious which can last for hours and progressive cognitive deficits. However, with regard to the influences of moderate TBI during children adulthood, injury-induced alterations of locomotive ability, long-term memory performance, and hippocampal electrophysiological firing changes have not yet been fully identified. In this study, lateral fluid percussion (LFP) method was used to fabricate moderate TBI in motor and somatosensory cortex of the 6-weeks-old mice. The motor function, learning and memory function, extracellular CA1 neural spikes were assessed during acute and subacute phase. Moreover, histopathology was performed on day post injury (DPI) 16 to evaluate the effect of TBI on tissue and cell morphological changes in cortical and hippocampal CA1 subregions. After moderate LFP injury, the 6-weeks-old mice showed severe motor deficits at the early stage in acute phase but gradually recovered later during adulthood. At the time points in acute and subacute phase after TBI, novel object recognition (NOR) ability and spatial memory functions were consistently impaired in TBI mice; hippocampal firing frequency and burst probability were hampered. Analysis of the altered burst firing shows a clear hippocampal theta rhythm drop. These electrophysiological impacts were associated with substantially lowered NOR preference as compared to the sham group during adulthood. These results suggest that moderate TBI introduced at motorsenory cortex in 6-weeks-old mice causes obvious motor and cognitive deficits during their adulthood. While the locomotive ability progressively recovers, the cognitive deficits persisted while the mice mature as adult mice. The cognitive deficits may be attributed to the general suppressing of whole neural network, which could be labeled by marked reduction of excitability in hippocampal CA1 subregion.

Highlights

  • traumatic brain injury (TBI) is a significant global public health problem and is a common condition affecting children all over the world [1, 2]

  • Juvenile rats who suffered either repeat mild TBI or moderate TBI revealed marked overall loss of neurons within cortical regions, including the motor and smatosensory cortex [7, 8]. These clinical and experimental observations suggested that frontal white matter tracts were highly vulnerable to pediatric TBI, the reduced microstructural integrity of the cortical and subregion connection, may act as a neuropathological mechanism contributing to TBI induced cognitive deficits

  • The primary damage of moderate/severe TBI can occur in specific brain areas; motor and somatosensory cortices are among the most vulnerable targets in patient suffered moderate/ severe TBI with diffuse axonal injury

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Summary

Introduction

TBI is a significant global public health problem and is a common condition affecting children all over the world [1, 2]. Juvenile rats who suffered either repeat mild TBI or moderate TBI revealed marked overall loss of neurons within cortical regions, including the motor and smatosensory cortex [7, 8]. These clinical and experimental observations suggested that frontal white matter tracts were highly vulnerable to pediatric TBI, the reduced microstructural integrity of the cortical and subregion connection, may act as a neuropathological mechanism contributing to TBI induced cognitive deficits

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