1. Acute demyelination disrupts the molecular organization of peripheral nervous system nodes.
- Author
-
Arroyo EJ, Sirkowski EE, Chitale R, and Scherer SS
- Subjects
- Acute Disease, Animals, Cell Communication, Cell Membrane pathology, Cell Membrane ultrastructure, Demyelinating Diseases chemically induced, Demyelinating Diseases physiopathology, Disease Models, Animal, Immunohistochemistry, Kv1.1 Potassium Channel, Lysophosphatidylcholines, Membrane Proteins metabolism, Microfilament Proteins, Microscopy, Electron, Transmission, Myelin Sheath metabolism, Myelin Sheath pathology, Myelin Sheath ultrastructure, Nerve Degeneration chemically induced, Nerve Degeneration metabolism, Nerve Degeneration physiopathology, Peripheral Nerves pathology, Peripheral Nerves physiopathology, Potassium Channels, Voltage-Gated metabolism, Ranvier's Nodes pathology, Ranvier's Nodes ultrastructure, Rats, Rats, Sprague-Dawley, Schwann Cells pathology, Schwann Cells ultrastructure, Cell Membrane metabolism, Demyelinating Diseases metabolism, Peripheral Nerves metabolism, Ranvier's Nodes metabolism, Schwann Cells metabolism
- Abstract
Intraneurally injected lysolecithin causes both segmental and paranodal demyelination. In demyelinated internodes, axonal components of nodes fragment and disappear, glial and axonal paranodal and juxtaparanodal proteins no longer cluster, and axonal Kv1.1/Kv1.2 K+ channels move from the juxtaparanodal region to appose the remaining heminodes. In paranodal demyelination, a gap separates two distinct heminodes, each of which contains the molecular components of normal nodes; paranodal and juxtaparanodal proteins are properly localized. As in normal nodes, widened nodal regions contain little or no band 4.1B. Lysolecithin also causes "unwinding" of paranodes: The spiral of Schwann cell membrane moves away from the paranodes, but the glial and axonal components of septate-like junctions remain colocalized. Thus, acute demyelination has distinct effects on the molecular organization of the nodal, paranodal, and juxtaparanodal region, reflecting altered axon-Schwann cell interactions.
- Published
- 2004
- Full Text
- View/download PDF