Degeneration of neural cells in the central nervous system of mice deficient in the gene for the adhesion molecule on glia, the β2 subunit of murine Na,K-ATPase

Josef Peter Magyar, Udo Bartsch, Zhao Qi Wang, Norma Howells, Adriano Aguzzi, Erwin F. Wagner, Melitta Schachner

Research output: Contribution to journalArticlepeer-review

85 Scopus citations

Abstract

We generated mice, null mutant in the adhesion molecule on glia (AMOG), the β2 subunit of the murine Na,K-ATPase gene. These mice exhibit motor incoordination at 15 d of age, subsequently tremor and paralysis of extremities, and die at 17-18 d after birth. At these ages, the mutants have enlarged ventricles, degenerating photoreceptor cells, and swelling and degeneration of astrocytic endfeet, leading to vacuoles adjoining capillaries of brain stem, thalamus, striatum, and spinal cord. In tissue homogenates from entire brains of 16-17-d-old mutants, Na,K-ATPase activity and expression of the β1 subunit of the Na,K-ATPase and of the neural adhesion molecules L1, N-CAM, and MAG appear normal. We suggest that the mutant phenotype can be related primarily to reduced pump activity, with neural degeneration as a possible consequence of osmotic imbalance.

Original languageEnglish (US)
Pages (from-to)835-845
Number of pages11
JournalJournal of Cell Biology
Volume127
Issue number3
DOIs
StatePublished - 1994
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cell Biology

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