Dynamics of Apoptotic and Necrotic Cell Death in Neurons and Glial Cells Sensorimotor Area Following Severe Traumatic Brain Injury
Elmira Mamytova1
1Neurology and Clinical Genetics, Kyrgyz State Medical Academy
Objective:

to examine the dynamics and nature of the regenerative and destructive processes that occur in the rat cerebral cortex depending on the severity and period of the traumatic brain injury.

Background:
Traumatic brain injury (TBI) causes progressive atrophy of brain tissue and subsequent neurological deficit, which is the result of neuronal death in humans and experimental animals. Traumatic brain injury is extremely difficult to study and mechanism of selective valnerability of individual groups of neurons to necrosis or apoptosis after TBI, still remains unclear.
Design/Methods:

The experiments were carried out on 36 adult mice weighing 180–220 g. There was used improved weight falling model of an experimental trauma. The sham group included all procedures except the trauma. The«trauma» group of mice had severe traumatic brain injury. To assess the severity of the TBI model, histological data, animal survival rates, and motor and cognitive dysfunctions were examined. Both light and electron microscopy were used to study the animal brains in each group.

Results:

Most dystrophic neuronal changes in mice with severe TBI were in contusion core between 1 and 21 days after the injury. Electronic microscopy revealed acute neuronal swelling, hydropic dystrophy of nerve cells with clear cytoplasmic vacuolization, localized and complete chromatolysis, hyperchromatism, and homogeneous cytoplasm. Detectable cellular reactions in the form of apoptosis of neurons and glial cell elements were observed in perifocal area from day 7 and were maximally noticeable on 21 day. The phenomena of regeneration of elements of nervous tissue during the observed period were not observed.

Conclusions:

Brain tissue lesions develop in the early stages of a TBI through rapid necrotic cell death. When developing neuroprotective strategies, it is necessary to take into account the temporal and spatial profiles of cell death of neurons and glial populations.

10.1212/WNL.0000000000204508