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Specific Expression of <i>N</i>‐Acetylaspartate in Neurons, Oligodendrocyte‐Type‐2 Astrocyte Progenitors, and Immature Oligodendrocytes In Vitro

508

Citations

34

References

1992

Year

TLDR

The study tests whether N‑acetylaspartate (NAA) can serve as a specific neuronal marker in 1H NMR spectroscopy by analyzing cultured cell types. Purified cultures of cerebellar granule neurons, type‑1 astrocytes, meningeal cells, O‑2A progenitor cells, and oligodendrocytes were assayed for NAA by 1H NMR and HPLC. NAA was abundant in cerebellar granule neurons, absent in astrocytes, meningeal cells, and mature oligodendrocytes, but present at twice neuronal levels in O‑2A progenitors and in immature oligodendrocytes, indicating that while NAA can mark neurons, its presence in oligodendroglial precursors suggests it may also reflect oligodendrocyte development.

Abstract

Abstract To test the specificity of N ‐acetylaspartate (NAA) as a neuronal marker for proton nuclear magnetic resonance ( 1 H NMR) spectroscopy, purified and characterized cultured cells were analyzed for their NAA content using both 1 H NMR and HPLC. Cell types studied included cerebellar granule neurons, type‐1 astrocytes, meningeal cells, oligodendrocyte‐type‐2 astrocyte (O–2A) progenitor cells, and oligodendrocytes. A high concentration of NAA was found in extracts of cerebellar granule neurons (approximately 12 nmol/mg of protein), whereas NAA remained undetectable in purified type‐1 astrocytes, meningeal cells, and mature oligodendrocytes. However, twice the neuronal level of NAA was found in O‐2A progenitors grown in vitro. In addition significant levels of NAA were also detected in cultures of immature oligodendrocytes. Our data partly support previous suggestions that NAA may be a useful neuronal marker for 1 H NMR spectroscopic examination of the adult brain. However, they also raise the further possibility that alterations of NAA associated with some specific brain disorders, particularly disorders seen in newborn and young children, may reflect abnormalities in the development of oligodendroglia or their precursors.

References

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1985

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1980

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1979

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1983

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1972

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1982

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1978

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1983

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