ISSN:
1573-7365
Keywords:
cerebral ischemia
;
protein synthesis
;
ribosomal RNA
;
amyloid A4 precursor protein
;
cytochromec oxidase
;
β-actin
;
in situ hybridization
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Brief periods of cerebreal ischemia result in prolonged inhibition of protein synthesis. In CAl sector of hippocampus inhibition is irreversible, leading to delayed death of pyramidal neurons. In order to study the possible role of gene transcription in this process, expression of four individual RNAs was investigated in the gerbil brain after 5 min of global cerebral ischemia byin situ hybridization with the following nucleic acid probes: plasmid pMr100 (ribosomal RNA sequences), plasmid pAG82 (cytochromec oxidase sequences), plasmid p629 (amyloid A4 precursor protein of Alzheimer's disease, pre-A4 protein), and plasmid pHFβA-1 (β-actin sequences). Cytochromec oxidase mRNA and ribosomal RNA did not show any changes in expression up to 48 hr after ischemia. After longer recirculation times they gradually declined in the CAl sector of hippocampus in parallel with the morphological manifestation of delayed neuronal death. The pre-A4 mRNA transiently decreased after 8 hr of recirculation of the CAl sector but then recovered before it finally disappeared in parallel with delayed neuronal death. Theβ-actin mRNA transiently appeared to increase after 8 hrof recirculation in the stratum radiatum of hippocampus but then also declined and disappeared when CAl neurons began to disintegrate. The possible significance of these changes in the pathogenesis of ischemic neuronal damage is discussed.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00999770
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