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Axo-glial interactions regulate the localization of axonal paranodal proteins.

Dupree JL, Girault JA, Popko B - J. Cell Biol. (1999)

Bottom Line: Using these mutants, we have analyzed the role that axo-glial interactions play in the establishment of axonal protein distribution in the region of the node of Ranvier.Whereas the clustering of the nodal proteins, sodium channels, ankyrin(G), and neurofascin was only slightly affected, the distribution of potassium channels and paranodin, proteins that are normally concentrated in the regions juxtaposed to the node, was dramatically altered.Paranodin/contactin-associated protein (Caspr), a paranodal protein that is a potential neuronal mediator of axon-myelin binding, was not concentrated in the paranodal regions but was diffusely distributed along the internodal regions.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.

ABSTRACT
Mice incapable of synthesizing the abundant galactolipids of myelin exhibit disrupted paranodal axo-glial interactions in the central and peripheral nervous systems. Using these mutants, we have analyzed the role that axo-glial interactions play in the establishment of axonal protein distribution in the region of the node of Ranvier. Whereas the clustering of the nodal proteins, sodium channels, ankyrin(G), and neurofascin was only slightly affected, the distribution of potassium channels and paranodin, proteins that are normally concentrated in the regions juxtaposed to the node, was dramatically altered. The potassium channels, which are normally concentrated in the paranode/juxtaparanode, were not restricted to this region but were detected throughout the internode in the galactolipid-defi- cient mice. Paranodin/contactin-associated protein (Caspr), a paranodal protein that is a potential neuronal mediator of axon-myelin binding, was not concentrated in the paranodal regions but was diffusely distributed along the internodal regions. Collectively, these findings suggest that the myelin galactolipids are essential for the proper formation of axo-glial interactions and demonstrate that a disruption in these interactions results in profound abnormalities in the molecular organization of the paranodal axolemma.

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Western blot analysis revealed no difference in the expression of paranodin between the wild-type (+/+) and the mutant (−/−) mice in either the spinal cord (S.C.) or the sciatic nerve (S.N.).
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Figure 3: Western blot analysis revealed no difference in the expression of paranodin between the wild-type (+/+) and the mutant (−/−) mice in either the spinal cord (S.C.) or the sciatic nerve (S.N.).

Mentions: In contrast, potassium channel distribution was dramatically altered in the CNS of the CGT-deficient mice. In the CNS and PNS of wild-type mice, intense labeling was commonly observed in the juxtaparanodal region (Fig. 1, a and c; Table ). The juxtaparanode was easily distinguished from the paranodal and nodal regions, since its diameter was conspicuously larger. Potassium channel antibody reactivity was occasionally observed in the paranodal region; however, the labeling intensity was greatly reduced. In the CNS of the mutant animals, fewer juxtaparanodal regions were immunolabeled with the Kv1.1 antibody (Fig. 1 b), whereas diffuse labeling over long stretches of axons was occasionally observed (see Fig. 3 b). When paranodal/juxtaparanodal potassium channel accumulations were present, the width of the labeling pattern did not change, indicating that the diameter of these axons does not change at the interface between the paranode and juxtaparanode in the galactolipid-deficient mice. In the PNS, paranodal/juxtaparanodal regions were typically labeled, although the labeling was frequently less intense and more diffuse as compared with the wild-type sciatic nerve fibers (Fig. 1c and Fig. d).


Axo-glial interactions regulate the localization of axonal paranodal proteins.

Dupree JL, Girault JA, Popko B - J. Cell Biol. (1999)

Western blot analysis revealed no difference in the expression of paranodin between the wild-type (+/+) and the mutant (−/−) mice in either the spinal cord (S.C.) or the sciatic nerve (S.N.).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2168103&req=5

Figure 3: Western blot analysis revealed no difference in the expression of paranodin between the wild-type (+/+) and the mutant (−/−) mice in either the spinal cord (S.C.) or the sciatic nerve (S.N.).
Mentions: In contrast, potassium channel distribution was dramatically altered in the CNS of the CGT-deficient mice. In the CNS and PNS of wild-type mice, intense labeling was commonly observed in the juxtaparanodal region (Fig. 1, a and c; Table ). The juxtaparanode was easily distinguished from the paranodal and nodal regions, since its diameter was conspicuously larger. Potassium channel antibody reactivity was occasionally observed in the paranodal region; however, the labeling intensity was greatly reduced. In the CNS of the mutant animals, fewer juxtaparanodal regions were immunolabeled with the Kv1.1 antibody (Fig. 1 b), whereas diffuse labeling over long stretches of axons was occasionally observed (see Fig. 3 b). When paranodal/juxtaparanodal potassium channel accumulations were present, the width of the labeling pattern did not change, indicating that the diameter of these axons does not change at the interface between the paranode and juxtaparanode in the galactolipid-deficient mice. In the PNS, paranodal/juxtaparanodal regions were typically labeled, although the labeling was frequently less intense and more diffuse as compared with the wild-type sciatic nerve fibers (Fig. 1c and Fig. d).

Bottom Line: Using these mutants, we have analyzed the role that axo-glial interactions play in the establishment of axonal protein distribution in the region of the node of Ranvier.Whereas the clustering of the nodal proteins, sodium channels, ankyrin(G), and neurofascin was only slightly affected, the distribution of potassium channels and paranodin, proteins that are normally concentrated in the regions juxtaposed to the node, was dramatically altered.Paranodin/contactin-associated protein (Caspr), a paranodal protein that is a potential neuronal mediator of axon-myelin binding, was not concentrated in the paranodal regions but was diffusely distributed along the internodal regions.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.

ABSTRACT
Mice incapable of synthesizing the abundant galactolipids of myelin exhibit disrupted paranodal axo-glial interactions in the central and peripheral nervous systems. Using these mutants, we have analyzed the role that axo-glial interactions play in the establishment of axonal protein distribution in the region of the node of Ranvier. Whereas the clustering of the nodal proteins, sodium channels, ankyrin(G), and neurofascin was only slightly affected, the distribution of potassium channels and paranodin, proteins that are normally concentrated in the regions juxtaposed to the node, was dramatically altered. The potassium channels, which are normally concentrated in the paranode/juxtaparanode, were not restricted to this region but were detected throughout the internode in the galactolipid-defi- cient mice. Paranodin/contactin-associated protein (Caspr), a paranodal protein that is a potential neuronal mediator of axon-myelin binding, was not concentrated in the paranodal regions but was diffusely distributed along the internodal regions. Collectively, these findings suggest that the myelin galactolipids are essential for the proper formation of axo-glial interactions and demonstrate that a disruption in these interactions results in profound abnormalities in the molecular organization of the paranodal axolemma.

Show MeSH
Related in: MedlinePlus