Microglial MHC antigen expression after ischemic and kainic acid lesions of the adult rat hippocampus
Identifieur interne : 000751 ( Main/Exploration ); précédent : 000750; suivant : 000752Microglial MHC antigen expression after ischemic and kainic acid lesions of the adult rat hippocampus
Auteurs : B. R. Finsen [Danemark] ; M. B. J Rgensen [Danemark] ; N. H. Diemer [Danemark] ; J. Zimmer [Danemark]Source :
- Glia [ 0894-1491 ] ; 1993-01.
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Abstract
By taking advantage of the specific neuronal and connective organization of the hippocampus and the different susceptibility of hippocampal neurons to transient cerebral ischemia or intraventricular injections of kainic acid (KA), we examined the microglial reactions to different types of neuronal injury. In all areas with neuronal or axonal degeneration, the microglial cells reacted by specific degeneration‐related morphological transformations and expression of class I major histocompatibility complex (MHC) antigen. Subpopulations of microglial cells also expressed class II MHC antigen and leukocyte common antigen (LCA) in relation to (1) degenerating nerve cell bodies in the dentate hilus and the CA1 and CA3 pyramidal cell layers, (2) postischemic degeneration of dendrites in the stratum radiatum of CA1, and (3) combined dendritic and axonal degeneration in the stratum radiatum of the KA‐lesioned CA3. MHC II and LCA expression was not observed in relation to degeneration of the CA3‐derived Schaffer collaterals in CA1 after KA‐induced CA3 lesions. In the case of ischemia the degeneration‐related reactions were preceded by an early, generalized microglial reaction, which also included areas without subsequent signs of neural degeneration. This reaction, which was transient and characterized by subtle morphological changes and induction of class I MHC antigen only, was presumably triggered by a general postischemic pertubation of the cerebral microenvironment, and not by actual neural degeneration. In conclusion, we found that microglial expression of class I MHC antigen was a sensitive marker of both the general pertubation after ischemia and axonal degeneration distant from the areas of actual nerve cell death. Induction of microglial LCA and class II MHC antigen expression, together with protracted expression of class I, was, characteristic of a protracted reaction, only found in areas with degeneration of nerve cell bodies and dendrites.
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DOI: 10.1002/glia.440070109
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In all areas with neuronal or axonal degeneration, the microglial cells reacted by specific degeneration‐related morphological transformations and expression of class I major histocompatibility complex (MHC) antigen. Subpopulations of microglial cells also expressed class II MHC antigen and leukocyte common antigen (LCA) in relation to (1) degenerating nerve cell bodies in the dentate hilus and the CA1 and CA3 pyramidal cell layers, (2) postischemic degeneration of dendrites in the stratum radiatum of CA1, and (3) combined dendritic and axonal degeneration in the stratum radiatum of the KA‐lesioned CA3. MHC II and LCA expression was not observed in relation to degeneration of the CA3‐derived Schaffer collaterals in CA1 after KA‐induced CA3 lesions. In the case of ischemia the degeneration‐related reactions were preceded by an early, generalized microglial reaction, which also included areas without subsequent signs of neural degeneration. This reaction, which was transient and characterized by subtle morphological changes and induction of class I MHC antigen only, was presumably triggered by a general postischemic pertubation of the cerebral microenvironment, and not by actual neural degeneration. In conclusion, we found that microglial expression of class I MHC antigen was a sensitive marker of both the general pertubation after ischemia and axonal degeneration distant from the areas of actual nerve cell death. Induction of microglial LCA and class II MHC antigen expression, together with protracted expression of class I, was, characteristic of a protracted reaction, only found in areas with degeneration of nerve cell bodies and dendrites.</div></front></TEI><affiliations><list><country><li>Danemark</li></country></list><tree><country name="Danemark"><noRegion><name sortKey="Finsen, B R" sort="Finsen, B R" uniqKey="Finsen B" first="B. R." last="Finsen">B. R. 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