Schwann Cells Modify Expression of Acetylcholinesterase and Butyrylcholinesterase at Rat Neuromuscular Junctions

Chapron, Jacqueline; Porte, Sabine de la; Delepine, Laurent; Koenig, Jeanine

doi:10.1111/j.1460-9568.1997.tb01396.x

Cited by 10 publications

(11 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A large fraction of OLN-93 cells also present significant levels of AChE immunoreactivity (not shown). Schwann cells at the neuromuscular junction also express both types of cholinesterases (Chapron et al, 1997). After antisense BChE transfection, BChE gene expression was efficiently lowered, as shown by immunoreactivity and Northern blots (not shown).…”

Section: Bche In Oln-93 Cells Acts By a Nonenzymatic Mechanismmentioning

confidence: 93%

“…For example, the enzyme is found accumulated at the blood-brain barrier interface (Joo and Csillik, 1966;Ciani, 1984;Risau and Wolburg, 1990), most likely due to its production by astroglial cells. In primary Schwann cell cultures of the chick sciatic nerve, BChE is expressed at significant levels (Weiss et al, 1996;Chapron et al, 1997). Moreover, in Mü ller cells of the developing chick retina, BChE expression is spatiotemporally regulated (Reiss et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Regulation of the rat oligodendroglia cell line OLN‐93 by antisense transfection of butyrylcholinesterase

Robitzki

Döll

Richter‐Landsberg

et al. 2000

Glia

View full text Add to dashboard Cite

Butyrylcholinesterase (BChE) is a glial cell marker with unknown function. For neuroepithelial cells, BChE has been shown to regulate cell division and expression of the postmitotic marker acetylcholinesterase (AChE), while similar studies are lacking for glial cells. By transducing an antisense‐5′BChE cDNA expression vector via calcium phosphate precipitation, we have analyzed the effect of BChE inhibition on proliferation and differentiation of rat oligodendroglia‐derived OLN‐93 cells. OLN‐93 cells were chosen because they are highly proliferative, while expressing markers of differentiated oligodendrocytes (Richter‐Landsberg and Heinrich, 1996). First, we established that OLN‐93 cells do express BChE protein, albeit chiefly in an inactive state, and that BChE was decreased by antisense‐5′BChE transfection. Cell proliferation was also strongly diminished, protein kinase C (PKCα) was upregulated, and expression of cytoskeletal and cell surface proteins was altered. In particular, immunoreactivities of the intermediate filament proteins vimentin and the cell adhesion protein F11 were detected, indicating that BChE‐inhibited OLN‐93 cells have shifted toward an astrocytic phenotype. These data support a role of the glia marker BChE in CNS glial cell proliferation and differentiation, achieved via a nonenzymatic mechanism. The possible biomedical impact of BChE protein, e.g., on CNS nerve regeneration, is briefly discussed. GLIA 31:195–205, 2000. © 2000 Wiley‐Liss, Inc.

show abstract

Section: Bche In Oln-93 Cells Acts By a Nonenzymatic Mechanismmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Regulation of the rat oligodendroglia cell line OLN‐93 by antisense transfection of butyrylcholinesterase

Robitzki

Döll

Richter‐Landsberg

et al. 2000

Glia

View full text Add to dashboard Cite

show abstract

“…This method allows the visualization of AChE patches as a stable signal and is therefore more adapted than immunofluorescence against AChE to measure the length of a large number of AChE patches. In neuron–myotube cocultures, synaptic patches of cholinesterase revealed a much stronger AChE than butyrylcholinesterase activity (Chapron et al ., 1997). Therefore, synaptic cholinesterase patches were composed largely of AChE forms, with very few butyrylcholinesterase forms, and we chose to name them AChE patches.…”

Section: Methodsmentioning

confidence: 99%

Thrombin reduces MuSK and acetylcholine receptor expression along with neuromuscular contact size in vitro

Faraut¹,

Ravel‐Chapuis²,

Bonavaud³

et al. 2004

Eur J of Neuroscience

View full text Add to dashboard Cite

In the course of studies on thrombin and its inhibitor(s) in synaptic plasticity, we addressed the question of their roles in the formation of neuromuscular junctions (NMJ) and used a model of rat neuron-myotube cocultures. We report that the size of acetylcholinesterase (AChE) patches used as a marker of neuromuscular contacts was decreased in the presence of either thrombin or SFLLRN, the agonist peptide of the thrombin receptor PAR-1, whereas it was increased with hirudin, a specific thrombin inhibitor. In an attempt to relate these neuromuscular contact size variations to molecular changes, we studied muscle-specific tyrosine kinase receptor (MuSK), acetylcholine receptor (AChR) and rapsyn expression in the presence of thrombin. We showed that thrombin did not change rapsyn gene and protein expression. However, the expression of MuSK and surface AChR proteins was diminished in both myotube cultures and neuron-myotube cocultures. These reductions in protein expression were associated with a decrease in MuSK and AChR alpha-subunit gene expression in myotube cultures but not in neuron-myotube cocultures. Moreover, the expression of the AChR epsilon-subunit gene, specifically enhanced by neuron-released factors, was not modified by thrombin in neuron-myotube cocultures. This suggests that thrombin did not affect the expression of synaptic AChRs enhanced by neuron-released factors but rather reduced the level of extrasynaptic AChRs. Taken together, these results indicate that thrombin in balance with its inhibitor(s) could modulate the formation of neuromuscular contacts in vitro by affecting the expression of two essential molecules in NMJ postsynaptic differentiation, MuSK and AChR.

show abstract

“…A growing body of evidence suggests that synaptic glia, which include both TSCs that cover peripheral synapses and astrocytes that cover central synapses, are intimately involved in virtually every facet of synapses, from their genesis and differentiation to their long-term maintenance and function [Ullian et al, 2001;Koenig et al, 1998;Robitaille, 1998;Chapron et al, 1997;Trachtenberg and Thompson, 1997]. For example, recent evidence indicates that TSCs in mature muscle respond to denervation by extending processes which provide a substrate that promotes axonal reinnervation of denervated endplates [Reynolds and Wolf, 1992;Son and Thompson, 1995a, b;O'Malley et al, 1999;Love and Thompson, 1999;Koirala et al;.…”

Section: Introductionmentioning

confidence: 99%

Testosterone Regulates Terminal Schwann Cell Number and Junctional Size during Developmental Synapse Elimination

Jordan

Williams²

2001

Dev Neurosci

View full text Add to dashboard Cite

Previous work has shown that exposure to exogenous testosterone during synapse elimination permanently stabilizes synapses that would normally be lost in the androgen-sensitive levator ani (LA) muscle, indicating that testosterone is a potent stabilizing factor for developing LA synapses. Terminal Schwann cells (TSCs), which cap the neuromuscular junction, have also been implicated in the control of synaptic stability and may play a decisive role in the selective stabilization of synapses during synapse elimination. In this study, we begin to investigate the possible role of TSCs in the effect of testosterone on synapse elimination by determining whether testosterone influences their number. As the number of TSCs generally correlates with the size of endplates, we also measured endplate size. Male rats were castrated or sham gonadectomized at postnatal day (P) 7 and given capsules containing either testosterone or nothing. Three weeks later (P27–28), LA neuromuscular junctions (NMJs) were stained using immune and nonimmune markers. As expected, testosterone treatment during synapse elimination maintained synapses that would ordinarily be eliminated. In addition, we find that the size of LA endplates and the number of TSCs per LA junction were also increased by the testosterone treatment. However, testosterone significantly increased the number of TSCs on both singly and multiply innervated fibers, indicating that the effect of testosterone on the number of TSCs is not specific to its effect on synapse maintenance. Rather the testosterone-induced increase in the number of TSCs appears related to the size of LA NMJs, a relationship that has precedence.

show abstract

Schwann Cells Modify Expression of Acetylcholinesterase and Butyrylcholinesterase at Rat Neuromuscular Junctions

Cited by 10 publications

References 58 publications

Regulation of the rat oligodendroglia cell line OLN‐93 by antisense transfection of butyrylcholinesterase

Regulation of the rat oligodendroglia cell line OLN‐93 by antisense transfection of butyrylcholinesterase

Thrombin reduces MuSK and acetylcholine receptor expression along with neuromuscular contact size in vitro

Testosterone Regulates Terminal Schwann Cell Number and Junctional Size during Developmental Synapse Elimination

Contact Info

Product

Resources

About