Mild cardiopulmonary arrest promotes synaptic dysfunction in rat hippocampus

Cardiac arrest (CA) patients exhibit learning and memory disabilities. These deficits suggest that synaptic dysfunction may underlie such disabilities. The hypothesis of the present study was that synaptic dysfunction occurs following CA and that this precedes cell death. To test this hypothesis, we...

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Bibliographic Details
Published in:Brain research 2004-10, Vol.1024 (1), p.89-96
Main Authors: Dave, Kunjan R., Raval, Ami P., Prado, Ricardo, Katz, Laurence M., Sick, Thomas J., Ginsberg, Myron D., Busto, Raul, Pérez-Pinzón, Miguel A.
Format: Article
Language:English
Subjects:
Action Potentials - physiology
Animals
Biological and medical sciences
Blood Pressure - physiology
Cardiopulmonary arrest
Heart Arrest - physiopathology
Hippocampus
Hippocampus - physiopathology
In Vitro Techniques
Ischemia
Male
Medical sciences
Neurology
Pathophysiology
Rats
Rats, Sprague-Dawley
Synapses - physiology
Vascular diseases and vascular malformations of the nervous system
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Summary:Cardiac arrest (CA) patients exhibit learning and memory disabilities. These deficits suggest that synaptic dysfunction may underlie such disabilities. The hypothesis of the present study was that synaptic dysfunction occurs following CA and that this precedes cell death. To test this hypothesis, we used histopathological and electrophysiological markers in the hippocampus of rats subjected to CA. Evoked potentials (EP) were determined in the CA1 region of hippocampal slices harvested from animals subjected to CA or sham-operated rats by stimulating the Schaffer collaterals and recording in the CA1 pyramidal region. EP amplitudes were significantly attenuated by approximately 60% in hippocampal slices harvested from animals subjected to CA. Hippocampal slices harvested from sham rats exhibited normal long-term potentiation (LTP). In contrast, hippocampal slices harvested 24 h after CA exhibited no LTP response, even when no histopathological abnormalities were observed. These data suggest that synaptic dysfunction occurs before and without overt histopathology. We suggest that the synaptic dysfunction precedes and may be an early marker for delayed neuronal cell death in the hippocampus after CA.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2004.07.050