Involvement of NCAM in the effects of GDNF on the neurite outgrowth in the dopamine neurons

Cao, Junping; Wang, Hongjun; Yu, Jing-Kao; Yang, Hua; Xiao, Chengshan; Gao, Dianshuai

doi:10.1016/j.neures.2008.04.008

Cited by 35 publications

(27 citation statements)

References 26 publications

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“…It has been implicated in the migration of neural crest cells (Akitaya and Bronner-Fraser, 1992), neurite outgrowth (Doherty and Walsh, 1992), axonal fasciculation (Cremer et al, 1997), myelination (Palser et al, 2009), molecular organisation and modulation of synapses (Kiss and Muller, 2001) and myogenesis (Knudsen et al, 1990). NCAM interacts with other NCAM molecules on adjacent cells, as well with fibroblast growth factor receptor (FGFR) (Povlsen et al, 2003), adhesion molecule L1 (Horstkorte et al, 1993), ATP (Hubschmann and Skladchikova), glial cell line-derived neurotrophic factor (GDNF) (Cao et al, 2008), prion protein (PrP) (Schmitt-Ulms et al, 2001), TAG-1/axonin-1 (Milev et al, 1996), glucocorticoid receptor (Crossin et al, 1997), brain-derived neurotrophic factor (BDNF) (Vutskits et al, 2001), platelet-derived growth factor (PDGF) (Zhang et al, 2004) and extracellular matrix components, in particular chondroitin sulphate proteoglycans and heparin sulphate proteoglycans (Kallapur and Akeson, 1992). In most instances, the interaction is mediated via the N-terminal Ig-like domains.…”

Section: Ncam Biologymentioning

confidence: 99%

Neural cell adhesion molecules in brain plasticity and disease

Gnanapavan

Giovannoni

2013

Multiple Sclerosis and Related Disorders

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Section: Ncam Biologymentioning

confidence: 99%

Neural cell adhesion molecules in brain plasticity and disease

Gnanapavan

Giovannoni

2013

Multiple Sclerosis and Related Disorders

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“…Although the study did not define the precise mechanism(s) for the aging-related changes in the DAergic system, it did establish that genetic reductions in the Gfrα-1 receptor can contribute to degenerative changes observed in this system during the aging process. The neural cell adhesion molecule (NCAM) has been identified as an alternative signaling receptor for GDNF (Cao et al, 2008) and was found to be involved in the promotive effect of GDNF on neurite outgrowth in DA neuron cultures. However, our findings presented here unequivocally establishe the role for the GFRα-1 receptor in maintenance of DA neuron health with aging.…”

Section: Genetic Alterations Combined With Environmental Toxinsmentioning

confidence: 99%

A dual-hit animal model for age-related parkinsonism

Boger

Granholm

McGinty

et al. 2010

Progress in Neurobiology

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Parkinson's disease is a neurological disorder which afflicts an increasing number of individuals. If the wider complex of extrapyramidal symptoms referred to as “age-related parkinsonism” is included, the incidence is near 50% of the population above 80 years of age. This review summarizes recent studies from our laboratories as well as other research groups in the quest to explore the multi-faceted etiology of age-related neurodegeneration, in general, and degeneration of the substantia nigra dopaminergic neurons, in particular. Our work during recent years has focused on assessment of potential interactive effects of a reduction in glial cell line-derived neurotrophic factor (GDNF) and the aging process (intrinsic factors) and early neurotoxin exposure (an extrinsic factor) on dopamine (DA) systems and the behaviors they mediate. The guiding hypothesis directing the research to be described was that a combination of the two factors would exacerbate the decline in the DA transmitter system function that occurs during aging. The results obtained were consistent with the well-established aging-related decline in function and structure of neurons utilizing DA as a transmitter and motor function, and extended knowledge by establishing that the genetic reduction of Gdnf exacerbated these aging related changes. Thus, Gdnf reduction appears to increase the vulnerability of the DA neurons to the many different challenges associated with the aging process. Assessment of methamphetamine effects on young Gdnf+/− mice indicated that reduced GDNF availability increased the vulnerability of DA systems to this well-established neurotoxin. The work discussed in this review is consistent with earlier work demonstrating the importance of GDNF for maintenance of DA neurons and also provides a novel model for progressive DA degeneration and motor dysfunction.

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“…The receptor complex for the GDNF family of ligands is composed of a signaling component Ret tyrosine kinase and 1 of 4 glycosylphosphatidylinositol-linked high-affinity ligand binding components designated as GFRα1–GFRα4. Glial cell line–derived neurotrophic factor has been extensively studied, especially with regard to its influence on neuronal populations including dopaminergic, central noradrenergic, sensory, and motoneurons 1,4,9,17,19,20,29,35,39,52. Designated as one of the most potent motoneuron survival factors,17 GDNF promotes peripheral nerve regeneration in multiple experimental models 3,16,30,38…”

mentioning

confidence: 99%

The differential effects of pathway- versus target-derived glial cell line–derived neurotrophic factor on peripheral nerve regeneration

Magill¹,

Moore

Yan

et al. 2010

JNS

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Object Glial cell line–derived neurotrophic factor (GDNF) has potent survival effects on central and peripheral nerve populations. The authors examined the differential effects of GDNF following either a sciatic nerve crush injury in mice that overexpressed GDNF in the central or peripheral nervous systems (glial fibrillary acidic protein [GFAP]–GDNF) or in the muscle target (Myo-GDNF). Methods Adult mice (GFAP-GDNF, Myo-GDNF, or wild-type [WT] animals) underwent sciatic nerve crush and were evaluated using histomorphometry and muscle force and power testing. Uninjured WT animals served as controls. Results In the sciatic nerve crush, the Myo-GDNF mice demonstrated a higher number of nerve fibers, fiber density, and nerve percentage (p < 0.05) at 2 weeks. The early regenerative response did not result in superlative functional recovery. At 3 weeks, GFAP-GDNF animals exhibit fewer nerve fibers, decreased fiber width, and decreased nerve percentage compared with WT and Myo-GDNF mice (p < 0.05). By 6 weeks, there were no significant differences between groups. Conclusions Peripheral delivery of GDNF resulted in earlier regeneration following sciatic nerve crush injuries than that with central GDNF delivery. Treatment with neurotrophic factors such as GDNF may offer new possibilities for the treatment of peripheral nerve injury.

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Involvement of NCAM in the effects of GDNF on the neurite outgrowth in the dopamine neurons

Cited by 35 publications

References 26 publications

Neural cell adhesion molecules in brain plasticity and disease

Neural cell adhesion molecules in brain plasticity and disease

A dual-hit animal model for age-related parkinsonism

The differential effects of pathway- versus target-derived glial cell line–derived neurotrophic factor on peripheral nerve regeneration

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