Expression of CHL1 and L1 by Neurons and Glia Following Sciatic Nerve and Dorsal Root Injury

Zhang, Y.; Roslan, RJ; Lang, Doris; Schachner, Melitta; Lieberman, A. R.; Anderson, PN

doi:10.1006/mcne.2000.0852

Cited by 86 publications

(73 citation statements)

References 54 publications

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“…In DRG of adult rats neurons and SGCs contain at least two subtypes of CAMs, N-CAM and L1 [115]. Sciatic nerve crush caused an upregulation of N-CAM and CHL1 (which is a close homologue of L1) in both sensory neurons and SGCs [192], and it was suggested that this may contribute to sympathetic nerve sprouting. More recent work revealed that CAMs can function as receptors for glial cell line-derived neurotrophic factor (GDNF) [133].…”

Section: Sgcs and Neurotrophinsmentioning

confidence: 99%

Satellite glial cells in sensory ganglia: from form to function

Hanani

2005

Brain Research Reviews

648

744

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Section: Sgcs and Neurotrophinsmentioning

confidence: 99%

Satellite glial cells in sensory ganglia: from form to function

Hanani

2005

Brain Research Reviews

648

744

View full text Add to dashboard Cite

“…After injuries of the adult mouse CNS and peripheral nervous system, CHL1 is upregulated in its expression in both neurons and astrocytes (Chaisuksunt et al, 2000;Zhang et al, 2000;Rolf et al, 2003). The functional consequences of this posttraumatic response have, however, remained unknown.…”

Section: Introductionmentioning

confidence: 99%

Glial Scar Expression of CHL1, the Close Homolog of the Adhesion Molecule L1, Limits Recovery after Spinal Cord Injury

Jakovčevski

Wu²,

Karl³

et al. 2007

J. Neurosci.

Self Cite

113

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The Ig superfamily adhesion molecule CHL1, the close homolog of the adhesion molecule L1, promotes neurite outgrowth, neuronal migration, and survival in vitro. We tested whether CHL1, similar to its close homolog L1, has a beneficial impact on recovery from spinal cord injury using adult CHL1-deficient (CHL1 Ϫ/Ϫ ) mice and wild-type (CHL1 ϩ/ϩ ) littermates. In contrast to our hypothesis, we found that functional recovery, assessed by locomotor rating and video-based motion analyses, was improved in CHL1 Ϫ/Ϫ mice compared with wild-type mice at 3-6 weeks after compression of the thoracic spinal cord. Better function was associated with enhanced monoaminergic reinnervation of the lumbar spinal cord and altered pattern of posttraumatic synaptic rearrangements around motoneurons. Restricted recovery of wild-type mice was likely related to early and persistent (3-56 d after lesion) upregulation of CHL1 in GFAP-positive astrocytes at the lesion core. In both the intact spinal cord and cultured astrocytes, enhanced expression of CHL1 and GFAP was induced by application of basic fibroblast growth factor, a cytokine involved in the pathophysiology of spinal cord injury. This upregulation was abolished by inhibitors of FGF receptor-dependent extracellular signal-regulated kinase, calcium/calmodulin-dependent kinase, and phosphoinositide-3 kinase signaling pathways. In homogenotypic and heterogenotypic cocultures of neurons and astrocytes, reduced neurite outgrowth was observed only if CHL1 was simultaneously present on both cell types. These findings and novel in vitro evidence for a homophilic CHL1-CHL1 interaction indicate that CHL1 is a glial scar component that restricts posttraumatic axonal growth and remodeling of spinal circuits by homophilic binding mechanisms.

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“…One of these genes is L1, a homophilically and heterophilically binding cell surface protein of the immunoglobulin superfamily of cell recognition molecules that is involved in many aspects of nervous system development, including axon growth and synaptic plasticity (for review, see Haspel and Grumet, 2003). During peripheral nerve regeneration, L1 is expressed in motor neurons and Schwann cells (Martini and Schachner, 1988;Zhang et al, 2000). In the mammalian CNS, expression of L1 is increased in subpopulations of axotomized neurons only when their axons regrow into a permissive peripheral nerve graft (Zhang et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

L1.1 Is Involved in Spinal Cord Regeneration in Adult Zebrafish

Becker¹,

Lieberoth²,

Morellini³

et al. 2004

J. Neurosci.

159

178

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Adult zebrafish, in contrast to mammals, regrow axons descending from the brainstem after spinal cord transection. L1.1, a homolog of the mammalian recognition molecule L1, is upregulated by brainstem neurons during axon regrowth. However, its functional relevance for regeneration is unclear. Here, we show with a novel morpholino-based approach that reducing L1.1 protein expression leads to impaired locomotor recovery as well as reduced regrowth and synapse formation of axons of supraspinal origin after spinal cord transection. This indicates that L1.1 contributes to successful regrowth of axons from the brainstem and locomotor recovery after spinal cord transection in adult zebrafish.

show abstract

Expression of CHL1 and L1 by Neurons and Glia Following Sciatic Nerve and Dorsal Root Injury

Cited by 86 publications

References 54 publications

Satellite glial cells in sensory ganglia: from form to function

Satellite glial cells in sensory ganglia: from form to function

Glial Scar Expression of CHL1, the Close Homolog of the Adhesion Molecule L1, Limits Recovery after Spinal Cord Injury

L1.1 Is Involved in Spinal Cord Regeneration in Adult Zebrafish

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