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Amphoterin (P30, HMG-1) and RIP are early markers of oligodendrocytes in the developing rat spinal cord

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Journal of Neurocytology

Summary

We have determined the cellular localization of the neurite outgrowth-promoting protein, amphoterin (p30), within the developing rat spinal cord in order to gain insight into possible function(s). Both neurons and oligodendrocytes are labelled by anti-amphoterin antibodies in tissue sections. Double labelling confirmed that labelled non-neuronal cells were oligodendrocytes and not astrocytes. White matter cells labelled by anti-amphoterin were first apparent in the spinal cord at embryonic day 18 (E18). The spinal cord white matter was most densely populated by amphoterin immunoreactive oligodendrocytes during the first postnatal week. In the adult spinal cord anti-amphoterin-labelled oligodendrocytes were infrequent. Neuronal staining was not diminished in adult animals. We have identified multiple populations of developing oligodendrocytes in the rat spinal cord. Oligodendrocytes (or precursors) in the presumptive white matter at E20 are elongated, radially oriented cells. Some are amphoterin+ and Rip, while others are positive for both antigens. At the same age, a small number of process-bearing Rip+ cells are present in the grey matter. These morphologically and antigenically defined populations of cells could reflect different oligodendrocyte lineages, developmental stages, or different responses to environmental cues. While the function of amphoterin is unknown, the finding that amphoterin is expressed in numerous oligodendrocytes from late embryonic development suggests that amphoterin expression may be important in the early stages of oligodendrocyte maturation. The onset of amphoterin expression, prior to the expression of myelin-specific antigens, makes amphoterin a useful marker for studying oligodendrocyte development.

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Daston, M.M., Ratner, N. Amphoterin (P30, HMG-1) and RIP are early markers of oligodendrocytes in the developing rat spinal cord. J Neurocytol 23, 323–332 (1994). https://doi.org/10.1007/BF01188500

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  • DOI: https://doi.org/10.1007/BF01188500

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