Glial Cell Line-Derived Neurotrophic Factor is a Survival Factor for Isolectin B4-Positive, but not Vanilloid Receptor 1-Positive, Neurons in the Mouse

Zwick, Melissa; Davis, Brian M.; Woodbury, C. Jeffery; Burkett, John N.; Koerber, H. Richard; Simpson, James; Albers, Kathryn M.

doi:10.1523/jneurosci.22-10-04057.2002

Cited by 204 publications

(203 citation statements)

References 52 publications

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“…It is possible that exogenous rhGDNF acted on the unmyelinated axons in a manner similar to that proposed for NGF by Voyvodic's (1989). In a more recent study, when GDNF was overexpressed in the skin of transgenic mice, the numbers of both myelinated and unmyelinated axons were increased in the saphenous nerve (Zwick et al, 2002). The data obtained by Zwick et al (2002) suggest that target-derived excess GDNF may have rescued a population of unmyelinated sensory neurons that would normally undergo programmed cell death and induced myelination in a subpopulation of these axons.…”

Section: Myelination Of Small Axonsmentioning

confidence: 78%

Glial Cell Line-Derived Neurotrophic Factor Alters Axon Schwann Cell Units and Promotes Myelination in Unmyelinated Nerve Fibers

et al. 2003

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Glial cell line-derived neurotrophic factor (GDNF) plays an important role in the development and maintenance of a subset of dorsal root ganglion sensory neurons. We administered high-dose exogenous recombinant human GDNF (rhGDNF) daily to adult rats to examine its effect on unmyelinated axon-Schwann cell units in intact peripheral nerves. In rhGDNF-treated animals, there was a dramatic proliferation in the Schwann cells of unmyelinated fibers, which resulted in the segregation of many unmyelinated axons into a 1:1 relationship with Schwann cells and myelination of normally unmyelinated small axons. This study demonstrates that the administration of high doses of a growth factor to adult rats can change the phenotype of nerve fibers from unmyelinated to myelinated.

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Section: Myelination Of Small Axonsmentioning

confidence: 78%

Glial Cell Line-Derived Neurotrophic Factor Alters Axon Schwann Cell Units and Promotes Myelination in Unmyelinated Nerve Fibers

et al. 2003

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“…Due to the extensive IB4 processes that form post-rhizotomy (see following section), we used an alternate marker of nonpeptidergic primary afferents, P2X 3 (Vulchanova et al, 1998), to determine if these axons sprout in L1 mutants. The percentage of IB4 neurons that express P2X 3 ranges from 67-87% whereas 98% of P2X 3 -positive fibers express IB4; thus P2X 3 labels a subset of the IB4-positive primary afferents (Bradbury et al, 1998;Zwick et al, 2002). P2X 3 -immunoreactive axons terminate in lamina IIi in both genotypes (Fig.…”

Section: Absence Of Nonpeptidergic Sprouting Post-rhizotomymentioning

confidence: 92%

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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“…To identify genes dependent on Sox11 expression that may influence neurite growth in DRG neurons, we identified genes that have Sox consensus binding domains in their proximal promoter region and whose expression was increased in developing sensory ganglia of transgenic animals that overexpress neurotrophic factors in the skin (Albers et al, 1994, Zwick et al, 2002. These overexpresser mice have enhanced axon growth and are known to express increased levels of Sox11 in developing sensory neurons (unpublished data).…”

Section: Possible Transcriptional Targets Of Sox11 In Cultured Drg Nementioning

confidence: 99%

SRY-box containing gene 11 (Sox11) transcription factor is required for neuron survival and neurite growth

et al. 2006

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The transcription factor Sox11 is expressed at high levels in developing sensory neurons and injured adult neurons but little is known about its transcriptional targets and function. In this study we examined the role of Sox11 using Neuro2a neuroblastoma cells and cultured mouse dorsal root ganglia (DRG) neurons. Results show Sox11 has an essential role in regulation of neuron survival and neurite outgrowth in Neuro2a cells and primary sensory neurons. Neuro2a cells increase expression of Sox11 as they differentiate in culture. Following addition of 20μM retinoic acid (RA), a stimulus for differentiation that enhances neurite growth and differentiation, Sox11 level rises. RNAi-mediated knockdown of Sox11 in RA-differentiated Neuro2a cells caused a decrease in neurite growth and an increase in the percent of apoptotic cells. RNA expression analysis showed that Sox11 knockdown modulated the level of mRNAs encoding several genes related to cell survival and death. Further validation in the Neuro2a model showed Sox11 knockdown increased expression of the proapoptotic gene BNIP3 (Bcl2 interacting protein 1 NIP3) decreased expression of the anti-apoptotic gene TANK (TRAF family member-associated NFκB activator). Cultured primary DRG neurons also express Sox11 and treatment with Sox11 siRNA caused a significant decrease in neurite growth and branching and a decrease in mRNA encoding actin-related protein complex 3 (Arpc3), an actin organizing protein that may be involved in axon growth. The percent of apoptotic neurons also increased in cultures of DRG neurons treated with Sox11 siRNA. Similar to Neuro2a cells, a decrease in TANK gene expression occurred, suggesting at least some overlap in Sox11 transcriptional targets in Neuro2a and DRG neurons. These data are consistent with a central role for Sox11 in regulating events that promote neurite growth and neuron survival.

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Glial Cell Line-Derived Neurotrophic Factor is a Survival Factor for Isolectin B4-Positive, but not Vanilloid Receptor 1-Positive, Neurons in the Mouse

Cited by 204 publications

References 52 publications

Glial Cell Line-Derived Neurotrophic Factor Alters Axon Schwann Cell Units and Promotes Myelination in Unmyelinated Nerve Fibers

Glial Cell Line-Derived Neurotrophic Factor Alters Axon Schwann Cell Units and Promotes Myelination in Unmyelinated Nerve Fibers

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

SRY-box containing gene 11 (Sox11) transcription factor is required for neuron survival and neurite growth

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