Spinocerebellar Ataxia Type-1 (SCA-1) is an inherited neurodegenerative of the cerebellum caused by a mutant CAG polyglutamine repeat tract in the portion of the Sca1 gene that codes for the protein Ataxin-1. SCA-1 is frequently studied in mouse models. In almost any case of neurological injury, hypertrophy and proliferation of glial cells, called gliosis, is observed. Gliosis has potentially harmful effects on the pathology of neurological degeneration. In order to the effect of cytokine-mediated gliosis on SCA-1 mice, Lys-M-Cre IKKβFlox transgenic mice were created. These mice have conditional depletion of IKKβ in the cerebellar microglia, IKKβ is an enzyme necessary for NF-κB mediated cytokine production, and without it, cells do not produce pro-inflammatory cytokines. We examined the cerebella of Lys-M-Cre IKKβFlox mice through immunohistochemical staining, using microglia-specific marker IBA-1, astrocyte-specific markers GFAP and S-100, and Purkinje neuron-specific Calbindin. From IBA-1 analysis, we have found that the loss of IKKβ does not cause microglial activation. Calbindin analysis revealed that the cerebella of Lys-M-Cre IKKβFlox mice are morphologically similar and comparable to those that express IKKβ. GFAP and S-100 analysis demonstrated results in the astrocytes opposite of IKKβ depletion in microglia, which merits further analysis.
This research was supported by the Undergraduate Research Opportunities Program (UROP).
Immunohistochemical Analysis of Cerebella in Mice With Conditional Depletion of IKKβ in the Microglia.
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