Remodeling of neuromuscular junctions in adult mouse soleus

Wigston, Donald J.

doi:10.1523/jneurosci.09-02-00639.1989

Cited by 73 publications

(55 citation statements)

References 31 publications

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“…These sites were also filled in. This is consistent with a low level of synaptic remodeling in normal animals (Rich and Lichtman, 1989a;Wigston, 1989;Hill et al, 1991;.…”

Section: Sites That Have Undergone Synapse Elimination Can Be Identifsupporting

confidence: 87%

Axon Withdrawal during Synapse Elimination at the Neuromuscular Junction Is Accompanied by Disassembly of the Postsynaptic Specialization and Withdrawal of Schwann Cell Processes

1998

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Nerve terminal withdrawal is accompanied by a loss of acetylcholine receptors (AChRs) at corresponding postsynaptic sites during the process of synapse elimination at developing and reinnervated adult (Rich and Lichtman, 1989a) neuromuscular junctions. Aside from AChR and nerve terminal loss, however, the molecular and cellular alterations that occur at sites of elimination are unknown. To gain a better understanding of the cascade of events that leads to the disassembly of synaptic sites during the synapse elimination process, we surveyed the distribution of molecular elements of the postsynaptic specialization, the basal lamina, and supporting Schwann cells during the process of synapse elimination that occurs after reinnervation. In addition, quantitative techniques were used to determine the temporal order of disappearance of molecules that were lost relative to the loss of postsynaptic AChRs. We found that the dismantling of the postsynaptic specialization was inhomogeneous, with evidence of rapid dissolution of some aspects of the postsynaptic apparatus and slower loss of others. We also observed a loss of Schwann cell processes from sites of synapse elimination, with a time course similar to that seen for nerve terminal retraction. In contrast, all of the extracellular markers that we examined were lost slowly from sites of synapse loss. We therefore conclude that the synapse elimination process is synapse-wide, removing not only nerve terminals but also Schwann cells and many aspects of the postsynaptic apparatus. The disassembly occurs in a stereotyped sequence with some synaptic elements appearing much more stable than others.

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“…These sites were also filled in. This is consistent with a low level of synaptic remodeling in normal animals (Rich and Lichtman, 1989a;Wigston, 1989;Hill et al, 1991;.…”

Section: Sites That Have Undergone Synapse Elimination Can Be Identifsupporting

confidence: 87%

Axon Withdrawal during Synapse Elimination at the Neuromuscular Junction Is Accompanied by Disassembly of the Postsynaptic Specialization and Withdrawal of Schwann Cell Processes

1998

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“…Specifically, the sprouts seen at 5% of NMJs in wild-type muscle may reflect the result of spontaneous outgrowth and regression of terminal extensions, as has been previously observed at the mouse NMJ (45). Their increased adhesion to the muscle fiber surface by elevated embigin would stabilize sprouts that in its absence might regress, thus increasing their occurrence in the transgenic muscle.…”

Section: Discussionmentioning

confidence: 66%

A Novel Role for Embigin to Promote Sprouting of Motor Nerve Terminals at the Neuromuscular Junction

Lain

Carnejac

Escher

et al. 2009

Journal of Biological Chemistry

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Adult skeletal muscle accepts ectopic innervation by foreign motor axons only after section of its own nerve, suggesting that the formation of new neuromuscular junctions is promoted by muscle denervation. With the aim to identify new proteins involved in neuromuscular junction formation we performed an mRNA differential display on innervated versus denervated adult rat muscles. We identified transcripts encoding embigin, a transmembrane protein of the immunoglobulin superfamily (IgSF) class of cell adhesion molecules to be strongly regulated by the state of innervation. In innervated muscle it is preferentially localized to neuromuscular junctions. Forced overexpression in innervated muscle of a full-length embigin transgene, but not of an embigin fragment lacking the intracellular domain, promotes nerve terminal sprouting and the formation of additional acetylcholine receptor clusters at synaptic sites without affecting terminal Schwann cell number or morphology, and it delays the retraction of terminal sprouts following re-innervation of denervated endplates. Conversely, knockdown of embigin by RNA interference in wild-type muscle accelerates terminal sprout retraction, both by itself and synergistically with deletion of neural cell adhesion molecule. These findings indicate that embigin enhances neural cell adhesion molecule-dependent neuromuscular adhesion and thereby modulates neuromuscular junction formation and plasticity.

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“…Unlike similar synapses in mice (Lichtman et al, 1987;Wigston, 1989;Balice-Gordon and Lichtman, 1990;Hill and Robbins, 1991), frog junctions are highly dynamic even in normal intact muscles Chen et al, 1991;Langenfeld-Oster et al, 1993). Cases of apparent synapse elimination and formation of new polyneuronal innervation have been directly observed in frogs (Herrera and Werle, 1990;Herrera et al, 1991).…”

Section: Abstract: Reinnervation; Synaptic Plasticity; Synaptic Remomentioning

confidence: 99%

Precision of Reinnervation and Synaptic Remodeling Observed in Neuromuscular Junctions of Living Frogs

1996

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Repeated in vivo observations were used to study regenerated nerve terminals in neuromuscular junctions of the adult frog Rana pipiens. Sartorius junctions in living animals were stained with the fluorescent vital dye RH414 and viewed with video fluorescence microscopy. Each junction was observed in the intact muscle and then again 7, 10, and 13 weeks after nerve crush. At 13 weeks, junctions were determined to be mono-or polyneuronally innervated using intracellular recording. Between 7 and 13 weeks, most identified junctions were reinnervated less precisely and completely than described previously. Although some of the original synaptic gutters were reoccupied by regenerated terminal branches, other gutters were only partially occupied, and many appeared abandoned. Junctions showing precise recapitulation of original terminal arborizations comprised a small number of the total examined, as did those where reinnervation was very imprecise. Striking differences in the precision of reinnervation were found within the muscle such that distal terminals regenerated more precisely and completely than did proximal terminals. Terminals in reinnervated muscles were more dynamic than terminals in unoperated muscles over equivalent times. In singly innervated junctions, terminal growth was favored over regression. In doubly innervated junctions, regressive events were more common. Imprecise reinnervation is explained in terms of multisite innervation of muscle fibers and the activity dependence of synaptic stability. We hypothesize that when axons reinnervate the second or third junctions on a fiber, they do so less precisely, because the activity restored by reinnervation of the first junction renders later sites less attractive or less stable.

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Remodeling of neuromuscular junctions in adult mouse soleus

Cited by 73 publications

References 31 publications

Axon Withdrawal during Synapse Elimination at the Neuromuscular Junction Is Accompanied by Disassembly of the Postsynaptic Specialization and Withdrawal of Schwann Cell Processes

Axon Withdrawal during Synapse Elimination at the Neuromuscular Junction Is Accompanied by Disassembly of the Postsynaptic Specialization and Withdrawal of Schwann Cell Processes

A Novel Role for Embigin to Promote Sprouting of Motor Nerve Terminals at the Neuromuscular Junction

Precision of Reinnervation and Synaptic Remodeling Observed in Neuromuscular Junctions of Living Frogs

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