Competing processes of cell death and recovery of function following ischemic preconditioning in the gerbil

Dooley, Paul James (1997) Competing processes of cell death and recovery of function following ischemic preconditioning in the gerbil. Masters thesis, Memorial University of Newfoundland.

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    Available under License - The author retains copyright ownership and moral rights in this thesis. Neither the thesis nor substantial extracts from it may be printed or otherwise reproduced without the author's permission.
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Abstract

The goal of the present study was to determine the neuroprotective efficacy of ischemic preconditioning using behavioral, electrophysiological and histological endpoints at various time points up to 90 days postischemia. Gerbils were exposed to a brief, non-injurious episode of forebrain ischemia (1.5 min) on each of two consecutive days. Three days following this preconditioning procedure, the animals received a 5 min occlusion. Other animals underwent sham surgery or a 5 min occlusion without preconditioning. -- Ischemic preconditioning appeared to provide striking cellular preservation at both rostral (79.7 and 66.9% of sham) and posterior levels of hippocampus (94 and 78% of sham) at 3 and 10 days survival, respectively. However, in spite of the near normal number of CA1 neurons, animals displayed impairments in an open field test of habituation as well as reduced dendritic field potentials in the CA1 area. Additionally, in ischemic animals the basal and apical dendritic regions of CA1 were nearly devoid of the cytoskeletal protein microtubule associated protein 2 (MAP2). Staining levels of MAP2 in sham and ischemic animals were similar. -- With increasing survival time, both open field performance and CA1 dendritic field potential amplitude in the ischemic preconditioined animals recovered. During this time, however, CA1 cell death continued over the 90 day survival period (p<0.05, vs. sham). -- Ischemic preconditioning provides a significant degree of neuroprotection characterized by a complex interplay of protracted cell death and neuroplasticity (recovery of function). These competing processes are best elucidated using a combination of functional and histological endpoints as well as multiple and extended survival times (i.e. greater than 7-10 days).

Item Type: Thesis (Masters)
URI: http://research.library.mun.ca/id/eprint/1238
Item ID: 1238
Additional Information: Bibliography: leaves 57-78
Department(s): Medicine, Faculty of
Date: 1997
Date Type: Submission
Library of Congress Subject Heading: Cerebral ischemia--Treatment; Cells--Preservation; Brain damage--Prevention
Medical Subject Heading: Brain Ischemia--therapy; Cell Death; Recovery of Function

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