Changes in oxidative metabolism and memory and learning in an cerebral hypoperfusion model in rats.
BACKGROUND
Chronic hypoperfusion in rats produces memory and learning impairments due to permanent occlusion of commun carotid arteries (POCCA). Molecular mechanisms leading to behavioural disorders have been poorly studied. For this reason, the aim of the present study was to characterise oxidative metabolism disorders and their implications in memory and learning impairments.


METHODS
Superoxide dismutase (SOD) and catalase (CAT) activities were determined in cortex, hippocampus and striatum homogenates at 24 hours and at 22 days after the lesion. Haematoxylin-eosin staining and glial fibrillary acidic protein (GFAP) immunoreactivity were performed on coronal sections. Behavioural impairments were explored using the Morris water maze (MWM). Escape latencies were determined in all behavioural studies.


RESULTS
The lesion induced a significant increase (P<.01) in CAT activity in the cortex at 24 hours, while SOD activity was significantly higher (P<.01) in the cortex and hippocampus at 22 days. An intense vacuolization was observed in the cortex and striatum as a result of the lesion. A neuronal loss in the striatum and hippocampus was observed. The glial reaction increased in the cortex and striatum. Visual alterations were observed in the lesion group with the lowest evolution time (P<.001). Escape latencies, corresponding to MWM schemes for long-term and short-term memory evaluation increased significantly (P<.05) in both groups of lesioned animals.


CONCLUSIONS
It was concluded that changes in SOD and CAT activities indicate a possible implication of oxidative imbalance in the pathology associated with chronic cerebral hypoperfusion. In addition, the POCCA model in rats is useful for understanding mechanisms by which cerebral hypoperfusion produces memory and learning impairments.
Departamento de Virología, Laboratorio de Diagnóstico, Instituto de Medicina Tropical Pedro Kourí, La Habana, Cuba. ycastano@ipk.sld.cu
Y
Y
Castaño Guerrero
M E
ME
González Fraguela
I
I
Fernández Verdecia
I
I
Horruitiner Gutiérrez
S
S
Piedras Carpio
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000523:psychology*; D017536:Carotid Artery, Common / Q000473:pathology; D016893:Carotid Stenosis / Q000378:metabolism / Q000523:psychology; D007858:Learning / Q000502:physiology*; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008568:Memory / Q000502:physiology*; D009042:Motivation / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000187:drug effects; D010084:Oxidation-Reduction; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
D009419:Nerve Tissue Proteins; D013482:Superoxide Dismutase