Long-Term Deficits Following Cerebral Hypoxia–Ischemia in Four-Week-Old Rats: Correspondence between Behavioral, Histological, and Magnetic Resonance Imaging Assessments
| Autor: | U.I. Tuor, Simon Sydserff, P. Kozlowski, Thomas J. Hudzik, M. R. Del Bigio, K. Malisza |
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| Rok vydání: | 2001 |
| Předmět: |
Pathology
medicine.medical_specialty Cerebral arteries Synaptophysin Ischemia Striatum Hippocampal formation Sensitivity and Specificity Time Central nervous system disease White matter Developmental Neuroscience Neurofilament Proteins Predictive Value of Tests Forelimb Glial Fibrillary Acidic Protein medicine Animals Rats Wistar Neurologic Examination Neuronal Plasticity Behavior Animal medicine.diagnostic_test Age Factors Brain Recovery of Function Anatomy medicine.disease Magnetic Resonance Imaging Electric Stimulation Rats medicine.anatomical_structure Neurology Motor Skills Hypoxia-Ischemia Brain Conditioning Operant Functional magnetic resonance imaging Psychology Motor cortex |
| Zdroj: | Experimental Neurology. 167:272-281 |
| ISSN: | 0014-4886 |
| Popis: | We examined whether following a hypoxic–ischemic insult in young animals there are long-lasting functional deficits that correlate either to histological tissue damage or to potential compensatory plasticity changes. Four-week-old rats were subjected to an episode of cerebral hypoxia–ischemia (right carotid artery occlusion + 30 min of hypoxia) or a sham operation. In hypoxic–ischemic animals there were gross neurological deficits 1, 24, and 48 h postinsult with recovery by 1 week. Behavioral deficits were observed in both the acquisition and the performance of a response duration differentiation test and a fine motor control test (staircase test) 3 months after the hypoxia–ischemia. Functional magnetic resonance imaging studies demonstrated less activation in the sensory–motor cortex of hypoxic–ischemic animals in response to left vs right forepaw stimulation 4 months postinsult. Histological assessment delineated striatal, cortical, and hippocampal damage in the hypoxic–ischemic hemisphere and a reduction in cortical thickness, bilaterally. GFAP immunoreactivity was increased in injured striatum and cortex. Neurofilament heavy chain (NF200) immunoreactivity was normally most intense in white matter and decreased in areas of ipsilateral cortical damage. Synaptophysin immunoreactivity was reduced around areas of infarction and somewhat increased in adjacent undamaged striatum and in layer IV of parietal cortex. The histological damage or chronic degenerative changes could account for much of the variance in functional outcome detected with sensitive behavioral tests so that overall the compensatory or plasticity changes evident within the juvenile brain are rather modest. |
| Databáze: | OpenAIRE |
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