Showing papers by "Samuel K. Ludwin published in 1987"

Effect of Quinolinic Acid in the Nucleus Basalis Magnocellularis on Cortical High-Affinity Choline Uptake

Abstract: A transient 45% increase in cortical high-affinity choline uptake (HACU) was observed after an injection of quinolinic acid (QUIN) into the nucleus basalis magnocellularis (nbM) of the rat. This was followed by a steady decline in choline uptake, which resulted in a 46% decrease by day 7. Specific (3H]hemicholinium-3 binding to coronal brain sections showed a similar pattern following injections of QUIN into the nbM. The increase in cortical HACU elicited by QUIN appeared to be dose dependent.

Regeneration of myelin and oligodendrocytes in the central nervous system.

Abstract: Publisher Summary This chapter discusses the potential for the regeneration of central nervous system (CNS) myelin and its formative and supportive cell, the oligodendrocyte. Myelin is lost in a wide variety of clinical diseases, both as a primary event in diseases, such as multiple sclerosis, and in secondary lesions in which the primary damage is to axons and neurons. With the current interest in the regeneration of the CNS, a burgeoning amount of information on the regeneration of axon has evolved; even some information suggests that the neuron itself may be a more plastic cell than previously thought and may be capable of regeneration. Full regeneration of the CNS requires the regeneration of myelin, whether the latter has been lost as a primary or a secondary event, along with the necessary regeneration of any other neuroglial elements that have been lost. CNS remyelination can occur in mammals and may be extensive and complete in the right system. Successful remyelination depends on an adequate supply of oligodendrocytes, which may be produced by proliferation or regeneration.

Oligodendrocyte Proliferation: Its Relationship to Central Nervous System Remyelination

Abstract: In recent years, the time honored concept that the adult mammalian central nervous system is incapable of regeneration has been seriously challenged. Much of this work has been directed towards studying the regenerative capability of neurons and axons, and there has been some evidence to show that even mature neurons may be capable of cell division (1). The regeneration of neuroglia and their products, specifically myelin, has also been the subject of renewed interest. Central nervous system remyelination has always been contrasted with the situation in the peripheral nervous system where remyelination rapidly follows both Wallerian and primary demyelination, and where the remyelination is preceeded by a brisk proliferation of Schwann cells. At a clinical level the potential importance of remyelination is great, not only in the primary demyelinating diseases such as multiple sclerosis, but also in other destructive diseases where any future advances in stimulating a neuronal regeneration will have to be accompanied by remyelination. These problems of central nervous system remyelination and oligodendroglial proliferation are intimately associated. In the peripheral nervous system Schwann cell proliferation is an important aspect of remyelination. These problems of central nervous system remyelination and oligodendroglial proliferation are intimately associated. In the peripheral nervous system Schwann cell proliferation is an important aspect of remyelination. Common dogma has accepted that mature postmyelinated oligodendrocytes are incapable of division although it is well established that proliferation occurs not only in differentiated astrocytes (2) and microglia (3, 4, 5) but in certain mammals in the undifferentiated cells of the subependymal plate (6). This failure of oligodendrocyte proliferation has been cited as one of the reasons accounting for the limited remyelinative capacity of the central nervous system.