Sprouting adult CNS cholinergic axons express nile and associate with astrocytic surfaces expressing neural cell adhesion molecule

Chalmers, Gordon; Peterson, Daniel A.; Gage, Fred H.

doi:10.1002/(sici)1096-9861(19960722)371:2<287::aid-cne8>3.0.co;2-z

Cited by 25 publications

(10 citation statements)

References 71 publications

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“…However, other data show that reactive astrocytes can serve as a permissive substratum for axonal regeneration. If resting astrocytes produce low levels of nerve growth factor (NGF), reactive astrocytes have been reported to produce significantly larger amounts (Strauss et al, 1994; Wu et al, 1998) and NGF was shown to induce axonal sprouting in vivo (Chalmers et al, 1996). Furthermore, regenerating axons expressing the adhesion molecule L1 can be supported by reactive astrocytic processes expressing NCAM.…”

Section: The Janus Face Of Neuroinflammation and Its Contribution To mentioning

confidence: 99%

Inflammation in ALS and SMA: Sorting out the good from the evil

Papadimitriou¹,

Verche²,

Jacquier³

et al. 2010

Neurobiology of Disease

121

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Indices of neuroinflammation are found in a variety of diseases of the CNS including amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). Over the years, neuroinflammation, in degenerative disorders of the CNS, has evolved from being regarded as an innocent bystander accomplishing its housekeeping function secondary to neurodegeneration to being considered as a bona fide contributor to the disease process and, in some situations, as a putative initiator of the disease. Herein, we will review not only neuroinflammation in both ALS and SMA from the angle of neuropathology, but also from the angle of its potential role in the pathogenesis and treatment of these two dreadful paralytic disorders.

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Section: The Janus Face Of Neuroinflammation and Its Contribution To mentioning

confidence: 99%

Inflammation in ALS and SMA: Sorting out the good from the evil

Papadimitriou¹,

Verche²,

Jacquier³

et al. 2010

Neurobiology of Disease

121

View full text Add to dashboard Cite

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“…Among the neuroprotective effects of the glial scar are the physical isolation of the injured area or the internalization of β-amyloid peptides observed in Alzheimer's disease (Dong and Benveniste, 2001); release of nerve growth factor (NGF) that induces axonal sprouting (Strauss et al, 1994;Wu et al, 1998;Chalmers et al, 1996); and release of anti- Fig. 2.…”

Section: Astrocyte and Synapse Dysfunction: Implications For Neurologmentioning

confidence: 99%

Neuron–glia signaling: Implications for astrocyte differentiation and synapse formation

et al. 2011

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“…L1 is among several growth-associated genes that are upregulated by neurons after nervous system injury (Daniloff, et al, 1986;Chaisuksunt et al, 2000;Kubasak et al, 2005), however its effects are contradictory. Some studies suggest that L1 CAM reiterates its developmental role following injury, as it is upregulated on sprouting and regenerating axons in many models (Daniloff et al, 1986;Martini and Schachner, 1988;Miragall et al, 1989;Styren et al, 1995;Chalmers et al, 1996;Brook et al, 2000;Kubasak et al, 2005;Chen et al, 2007). However, other studies conclude that L1 is not essential for axonal growth into the injury site (Jakeman et al, 2006) and that nerve growth factor-induced sprouting is even reduced by co-expression of L1 (Chaudhry et al, 2006).…”

Section: Nih Public Accessmentioning

confidence: 99%

L1 cell adhesion molecule is not required for small-diameter primary afferent sprouting after deafferentation

Runyan

Roy²,

Zhong³

et al. 2007

Neuroscience

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L1 is a cell adhesion molecule associated with axonal outgrowth and fasciculation during spinal cord development and may reiterate its developmental role in adults following injury; L1 is upregulated on certain sprouting and regenerating axons in adults, but it is unclear if L1 expression is necessary for, or contributes to, regrowth of axons. This study asks if L1 is required for small-diameter primary afferents to sprout by conducting unilateral dorsal rhizotomies (6 segments; T10-L2) on both wildtype and L1 mutant mice. First we determined that L1 co-localizes substantially with the peptidergic (calcitonin gene-related peptide; CGRP) but minimally with the nonpeptidergic (isolectin B4; IB4) primary afferents in intact wild-type and L1 mutant mice. However, we encountered a complication using IB4 to identify primary afferents post-rhizotomy; we detected extensive abnormal IB4 expression in the dorsal horn and dorsal columns. Much of this aberrant IB4 labeling is associated with fibrous astrocytes and microglia. Five days after dorsal rhizotomy a large decrease in peptidergic and nonpeptidergic afferents is evident on the deafferented side in both wild-type and L1 mutants. Three months after surgery the peptidergic primary afferents sprouted into the center of the denervated dorsal horn in both wild-type and mutant mice, and quantitative analyses confirmed a sprouting density of similar magnitude in both genotypes. In contrast, we did not detect sprouting in the nonpeptidergic primary afferents in either genotype. These results suggest that the absence of L1 neither diminishes nor enhances sprouting of peptidergic small-diameter primary afferent axons following a dorsal rhizotomy. Keywordscell adhesion molecule; denervated; IB4; CGRP; nociceptors; rhizotomy The cell adhesion molecule L1 (L1 CAM) is an axonal glycoprotein and a member of the immunoglobulin superfamily (Kamiguchi et al., 1997). L1 plays a role in axonal outgrowth, fasciculation, and guidance during spinal cord development (Stallcup et al., 1985;Jessell, 1988;Stoeckli and Landmesser, 1995;Orlino et al., 2000;Tran and Phelps, 2000;Akopians et al., 2003) through homophilic and various heterophilic binding partners such as integrins (αVβ3 and α5β1) and the fibroblast growth factor receptor (Kamiguchi and Lemmon, 1997 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Lemmon, 1997;Castellani et al., 2000). NIH Public AccessMutations in X-linked L1 in humans cause major developmental errors and result in a group of symptoms that include corpus callosum hypoplasia, spastic paraplegia and hydrocephalus (Fran...

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Sprouting adult CNS cholinergic axons express nile and associate with astrocytic surfaces expressing neural cell adhesion molecule

Cited by 25 publications

References 71 publications

Inflammation in ALS and SMA: Sorting out the good from the evil

Inflammation in ALS and SMA: Sorting out the good from the evil

Neuron–glia signaling: Implications for astrocyte differentiation and synapse formation

L1 cell adhesion molecule is not required for small-diameter primary afferent sprouting after deafferentation

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