Fate of developing astrocytes in the optic nerve of the myelin-deficient rat

Struckhoff, Gernot; Przyrembel, C.; Bähr, Mathias; Gocht, Andreas

doi:10.1002/(sici)1096-9861(19970203)378:1<105::aid-cne6>3.0.co;2-8

Cited by 3 publications

(2 citation statements)

References 62 publications

(88 reference statements)

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“…There are two previous reports on the molecular organization of myelinated axons in md rats. The monoclonal antibody HNK-1 stains the optic nerve diffusely (Struckhoff et al, 1997), whereas it stains perinodal astrocytes in WT optic nerves (ffrench- Constant and Raff, 1986). Thus, we expected to find diffuse tenascin-R staining, because tenascin-R is the only molecule localized to perinodal astrocytes that has an HNK-1 epitope (ffrench-Constant et al, 1986).…”

Section: The Organization Axonal Proteins In Dysmyelinating Mutantsmentioning

confidence: 97%

Genetic Dysmyelination Alters the Molecular Architecture of the Nodal Region

et al. 2002

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We have examined the molecular organization of axons in the spinal cords of myelin-deficient (md) rats, which have profound CNS dysmyelination associated with oligodendrocyte cell death. Although myelin sheaths are rare, most large axons are at least partially surrounded by oligodendrocyte processes. At postnatal day 7 (P7), almost all node-like clusters of voltage-gated Na+ channels and ankyrinG are adjacent to axonal segments ensheathed by oligodendrocytes, but at P21, many node-like clusters are found in axonal segments that lack oligodendrocyte ensheathment. In P21 wild-type (WT) rats, the voltage-gated Na+ channels Na(v)1.2, Na(v)1.6, and Na(v)1.8, are found in different subpopulations of myelinated axons, and md rats have a similar distribution. The known molecular components of paranodes--contactin, Caspr, and neurofascin 155--are not clustered in md spinal cords, and no septate-like junctions between oligodendrocyte processes and axons are found by electron microscopy. Furthermore, Kv1.1 and Kv1.2 K+ channels are not spatially segregated from the node-like clusters of Na+ channels in md rats, in contrast to their WT littermates. These results suggest the following: node-like clusters of voltage-gated Na+ channels and ankyrinG form adjacent to ensheathed axonal segments even in the absence of a myelin sheath; these clusters persist after oligodendrocyte cell death; dysmyelination does not alter the expression of different nodal of voltage-gated Na+ channels; the absence of paranodes results in the mislocalization of neurofascin155, contactin, and Caspr, and the aberrant localization of Kv1.1 and Kv1.2.

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Section: The Organization Axonal Proteins In Dysmyelinating Mutantsmentioning

confidence: 97%

Genetic Dysmyelination Alters the Molecular Architecture of the Nodal Region

et al. 2002

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“…However, the presence of these two populations in the adult optic nerve or in other white matter regions of the CNS in vivo has not been confirmed (Butt et al. 1994a,b; Struckhoff et al. 1997).…”

Section: Astrocyte Heterogeneitymentioning

confidence: 99%

Determinants of regional and local diversity within the astroglial lineage of the normal central nervous system

Hewett

2009

Journal of Neurochemistry

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Astrocytes are a major component of the resident non‐neuronal glial cell population of the CNS. They are ubiquitously distributed throughout the brain and spinal cord, where they were initially thought to function in both structural and homeostatic capacities, providing the framework and environment in which neurons performed their parenchymal duties. However, this stroma‐like view of astrocytes is no longer satisfactory. Mounting evidence particularly within the last decade indicates that astrocytes do not simply support neuronal activity but directly contribute to it. Congruent with this evolving view of astrocyte function in information processing is the emergent notion that these glial cells are not a homogeneous population of cells. Thus, astrocytes in various anatomically distinct regions of the normal CNS possess unique phenotypic characteristics that may directly influence the particular neuronal activities that define these regions. Remarkably, regional populations of astrocytes appear to exhibit local heterogeneity as well. Many phenotypic traits of the astrocyte lineage are responsive to local environmental cues (i.e., are adaptable), suggesting that plasticity contributes to this diversity. However, compelling evidence suggests that astrocytes arise from multiple distinct progenitor pools in the developing CNS, raising the intriguing possibility that some astrocyte heterogeneity may result from intrinsic differences between these progenitors. The purpose of this review is to explore the evidence for and mechanistic determinants of regional and local astrocyte diversity.

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Group 1 mGlu receptors elevate [Ca2+]i in rat cultured cortical type 2 astrocytes: [Ca2+]i synergy with adenosine A1 receptors

Toms

Roberts

1999

Neuropharmacology

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Fate of developing astrocytes in the optic nerve of the myelin-deficient rat

Cited by 3 publications

References 62 publications

Genetic Dysmyelination Alters the Molecular Architecture of the Nodal Region

Genetic Dysmyelination Alters the Molecular Architecture of the Nodal Region

Determinants of regional and local diversity within the astroglial lineage of the normal central nervous system

Group 1 mGlu receptors elevate [Ca2+]i in rat cultured cortical type 2 astrocytes: [Ca2+]i synergy with adenosine A1 receptors

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