Cytoarchitectonics of the Sensorimotor Cortex and Hippocampal Field CA1 in White Rats with Different Levels of Convulsive Activity in the Post-Trauma Period
Autor: | V. V. Semchenko, E. Yu. Sokolov |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
medicine.medical_specialty business.industry General Neuroscience Period (gene) Hippocampus Hippocampal formation Craniocerebral trauma 03 medical and health sciences symbols.namesake 030104 developmental biology 0302 clinical medicine Endocrinology nervous system Cytoarchitecture Internal medicine Nissl body symbols medicine business Sensorimotor cortex Pathological 030217 neurology & neurosurgery |
Zdroj: | Neuroscience and Behavioral Physiology. 49:99-102 |
ISSN: | 1573-899X 0097-0549 |
DOI: | 10.1007/s11055-018-0700-7 |
Popis: | Objectives. To study the cytoarchitectonics of the sensorimotor cortex (SMC) in hippocampal field CA1 in white rats after severe craniocerebral trauma. Materials and methods. Multiple trauma was modeled using the Noble–Collip method under anesthesia. The study group (n = 25) included animals with convulsive paroxysms (CP) and the reference group (n = 25) included animals not displaying CP to trauma. Specimens were collected 1, 3, 7, 14, and 30 days after trauma. Sections were stained by the Nissl method and the total number density of pyramidal neurons (TNDN) was determined, along with the content of dark neurons (DN). Statistical hypotheses were tested in Statistica 8.0. Results. One day after trauma, the SMC and hippocampal field CA1 showed significant increases in the numbers of DN. In the late recovery period, 65.0% of DN in the SMC recovered to normochromic in the late recovery period, with 18% doing so in hippocampal field CA1. The occurrence of CP hindered recovery of DN: 54.5% recovered in the SMC and only 2.7% in hippocampal field CA1. As a result, TNDN in the SMC and hippocampus decreased by 32.4% and 55.6%, respectively, compared with decreases by 24.7% and 43.3%, respectively, in the reference group. Conclusions. CP appeared to be a factor increasing pathological changes in neurons in the posttrauma period. |
Databáze: | OpenAIRE |
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