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Bergmann glia require continuous association with Purkinje cells for normal phenotype expression
M Fisher1, P Trimmer, G Ruthel
1Department of Anatomy and Cell Biology, University of Virginia School of Medicine, Charlottesville 22908.
Glia
|July 1, 1993
Summary
Bergmann glia (Bg) down-regulate glycerol-3-phosphate dehydrogenase (GPDH) after Purkinje cell (Pc) loss. Re-establishing this interaction in young mice can sustain GPDH, but not reinduce it in older mice.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- Bergmann glia (Bg) are crucial cerebellar glial cells.
- Purkinje cells (Pc) normally regulate GPDH expression in Bg.
- Pc death in Lurcher (Lc) mutant mice leads to decreased GPDH in Bg.
Purpose of the Study:
- To investigate if adult Pcs maintain glial GPDH expression.
- To determine if Pcs can reinduce GPDH in Bergmann glia after downregulation.
- To explore the age and location dependency of Pc-glia interactions.
Main Methods:
- Purkinje cell (Pc) ablation in adult wild-type mice using kainic acid.
- Grafting of wild-type fetal Pcs into Lurcher (Lc) mutant mouse cerebella.
- Electron microscopy (EM) to analyze Bergmann glia (Bg) ensheathment of grafted Pcs.
Main Results:
- Pc loss in wild-type mice of all ages caused GPDH downregulation in Bg.
- GPDH reinduction by grafted Pcs was dependent on host age (younger than 6 weeks) and graft position.
- Bg ensheathment of grafted Pcs was thinner but qualitatively similar to normal.
Conclusions:
- The interaction between host Bergmann glia and Purkinje cells can sustain GPDH expression if not previously downregulated.
- This interaction is insufficient to reinduce GPDH in Bergmann glia that have already downregulated the enzyme.
- Age and location are critical factors in the efficacy of Purkinje cell-glia interactions for GPDH regulation.