Distinct Time Courses of Secondary Brain Damage in the Hippocampus Following Brain Concussion and Contusion in Rats

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  • Nakajima Yuko
    Department of Veterinary Medicine, Nihon University College of Bioresonance Bioresource Science
  • Horiuchi Yutaka
    Department of Veterinary Medicine, Nihon University College of Bioresonance Bioresource Science
  • Kamata Hiroshi
    Department of Veterinary Medicine, Nihon University College of Bioresonance Bioresource Science
  • Yukawa Masayoshi
    Department of Veterinary Medicine, Nihon University College of Bioresonance Bioresource Science
  • Kuwabara Masato
    Department of Veterinary Medicine, Nihon University College of Bioresonance Bioresource Science
  • Tsubokawa Takashi
    Department of Neurosurgery, Nihon University School of Medicine

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Secondary brain damage (SBD) is caused by apoptosis after traumatic brain injury that is classified into concussion and contusion. Brain concussion is temporary unconsciousness or confusion caused by a blow on the head without pathological changes, and contusion is a brain injury with hemorrhage and broad extravasations. In this study, we investigated the time-dependent changes of apoptosis in hippocampus after brain concussion and contusion using rat models. We generated the concussion by dropping a plumb on the dura from a height of 3.5 cm and the contusion by cauterizing the cerebral cortex. SBD was evaluated in the hippocampus by histopathological analyses and measuring caspase-3 activity that induces apoptotic neuronal cell death. The frequency of abnormal neuronal cells with vacuolation or nuclear condensation, or those with DNA fragmentation was remarkably increased at 1 hr after concussion (about 30% for each abnormality) from the pre-injury level (0%) and reached the highest level (about 50% for each) by 48 hrs, whereas the frequency of abnormal neuronal cells was increased at 1 hr after contusion (about 10%) and reached the highest level (about 40%) by 48 hrs. In parallel, caspase-3 activity was increased sevenfold in the hippocampus at 1 hr after concussion and returned to the pre-injury level by 48 hrs, whereas after contusion, caspase-3 activity was continuously increased to the highest level at 48 hrs (fivefold). Thus, anti-apoptotic-cell-death treatment to prevent SBD must be performed by 1 hr after concussion and at latest by 48 hrs after contusion.

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