Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Böttiger, BW; Teschendorf, P; Krumnikl, JJ; Vogel, P; Galmbacher, R; Schmitz, B; Motsch, J; Martin, E; Gass, P.
Global cerebral ischemia due to cardiocirculatory arrest in mice causes neuronal degeneration and early induction of transcription factor genes in the hippocampus.
Brain Res Mol Brain Res. 1999; 65(2): 135-142.
Doi: 10.1016/S0169-328X(98)00298-8
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- Co-Autor*innen der Med Uni Graz
- Krumnikl Jakub
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- Abstract:
- To analyze the role of specific genes and proteins in neuronal signaling cascades following global cerebral ischemia, it would be useful to have a reproducible model of global cerebral ischemia in mice that potentially allows the investigation of mice with specific genomic mutations. We first report on the development of a model of reversible cardiocirculatory arrest in mice and the consequences of such an insult to neuronal degeneration and expression of immediate early genes (IEG) in the hippocampus. Cardiocirculatory arrest of 5 min duration was induced via ventricular fibrillation in mechanically ventilated NMRI mice. After successful cardiopulmonary resuscitation (CPR), animals were allowed to reperfuse spontaneously for 3 h (n=7) and 7 days (n=7). TUNEL staining revealed a selective degeneration of a subset of neurons in the hippocampal CA1 sector at 7 days. About 30% of all TUNEL-positive nuclei showed condensed chromatin and apoptotic bodies. Immunohistochemical studies of IEG expression performed at 3 h exhibited a marked induction of c-Fos, c-Jun, and Krox-24 protein in all sectors of the hippocampus, peaking in vulnerable CA1 pyramidal neurons and in dentate gyrus. In contrast, sham-operated animals (n=3) did not reveal neuronal degeneration or increased IEG expression in the hippocampus when compared with untreated control animals (n=3). In conclusion, we present a new model of global cerebral ischemia and reperfusion in mice with the use of complete cardiocirculatory arrest and subsequent CPR. Following 5 min of ischemia, a subset of CA1 pyramidal neurons was TUNEL-positive at 7 days. The expression of IEG was observed in all sectors of the hippocampus, including selectively vulnerable CA1 pyramidal neurons. This appears to be a good model which should be useful in evaluating the role of various genes in transgenic and knockout mice following global ischemia.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Apoptosis - physiology
- Brain Ischemia - genetics
- Cerebrovascular Circulation - physiology
- Disease Models, Animal - physiology
- Electric Stimulation - physiology
- Gene Expression - physiology
- Genes, Immediate-Early - physiology
- Heart Arrest - physiopathology
- Hippocampus - blood supply
- In Situ Nick-End Labeling - blood supply
- Male - blood supply
- Mice - blood supply
- Mice, Inbred Strains - blood supply
- Nerve Degeneration - genetics
- Transcription Factors - genetics
- Find related publications in this database (Keywords)
- global cerebral ischemia
- cardiac arrest
- TUNEL staining
- immediate early gene
- mouse