Light and electron microscopic identification of nerve terminal sprouting and retraction in normal adult frog muscle.

Anzil, A. P.; Bieser, A.; Wernig, A.

doi:10.1113/jphysiol.1984.sp015207

Cited by 53 publications

(26 citation statements)

References 17 publications

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“…In contrast to the case in mice where the junctions appear stable through early adulthood (Balice-Gordon and Lichtman, 1990), frog junctions show considerable remodeling with seasons of the year, including regression of nerve terminals and SCs from portions of the synaptic contacts, with subsequent turnover of the AChR at the abandoned sites (Anzil et al, 1984). In addition, there is growth of terminals and SCs and deposition of AChR to establish new synaptic sites.…”

Section: Discussionmentioning

confidence: 87%

Terminal Schwann Cells Participate in Neuromuscular Synapse Remodeling during Reinnervation following Nerve Injury

et al. 2014

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Schwann cells (SCs) at neuromuscular junctions (NMJs) play active roles in synaptic homeostasis and repair. We have studied how SCs contribute to reinnervation of NMJs using vital imaging of mice whose motor axons and SCs are transgenically labeled with different colors of fluorescent proteins. Motor axons most commonly regenerate to the original synaptic site by following SC-filled endoneurial tubes. During the period of denervation, SCs at the NMJ extend elaborate processes from the junction, as shown previously, but they also retract some processes from territory they previously occupied within the endplate. The degree of this retraction depends on the length of the period of denervation. We show that the topology of the remaining SC processes influences the branching pattern of regenerating axon terminals and the redistribution of acetylcholine receptors (AChRs). Upon arriving at the junction, regenerating axons follow existing SC processes within the old synaptic site. Some of the AChR loss that follows denervation is correlated with failure of portions of the old synaptic site that lack SC coverage to be reinnervated. New AChR clustering is also induced by axon terminals that follow SC processes extended during denervation. These observations show that SCs participate actively in the remodeling of neuromuscular synapses following nerve injury by their guidance of axonal reinnervation.

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Section: Discussionmentioning

confidence: 87%

Terminal Schwann Cells Participate in Neuromuscular Synapse Remodeling during Reinnervation following Nerve Injury

et al. 2014

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“…In neuromuscular junctions, presynaptic terminals unapposed to postsynaptic specializations (newly formed terminals), and postsynaptic specializations unapposed by presynaptic terminals (regressing synapses) are normally seen (Wemig et al, 1980;Anzil et al, 1984;Wemig and Fisher, 1986), though the molecular mechanisms that might regulate this dynamic process are still unknown. In the present study, we only looked at neuromuscular junctions of third-instar larvae.…”

Section: Discussionmentioning

confidence: 99%

Morphological plasticity of motor axons in Drosophila mutants with altered excitability

1990

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An anatomical and electrophysiological study of Drosophila mutants has been made to determine the effect of altered electrical activity on the development and maintenance of larval neuromuscular junctions. We examined motor axon terminals of (1) hyperexcitable mutants Shaker (Sh), ether a go-go (eag), Hyperkinetic (Hk), and Duplication of para+ (Dp para+); and (2) mutants with reduced excitability, no action potential (napts) and paralytic (parats 1). Nerve terminals innervating larval body-wall muscles were visualized by using anti-HRP immunocytochemistry, which specifically stains neurons in insect species. In wild-type larvae, motor axon terminals were distributed in a stereotypic fashion. However, in combinations of eag and Sh alleles, the basic pattern of innervation was altered. There was an increase in both the number of higher-order axonal branches over the muscles and the number of varicosities on the neurites. A similar phenomenon was found in the double mutant Hk eag and, to a lesser extent, in Dp para+ and Dp para+ Sh mutants. It is known that at permissive temperature the napts, but not parats 1, mutation decreases excitability of larval motor axons and suppresses the behavioral phenotypes of Sh, eag, and Hk. In the mutant napts (reared at permissive temperature), a slight decrease in the extent of branching was observed. Yet, when combined with eag Sh, napts completely reversed the morphological abnormality in eag Sh mutants. No such reversion was observed in parats 1 eag Sh mutants. The endogenous patterns of electrical activity at the neuromuscular junction were analyzed by extracellular recordings in a semi-intact larval preparation. Recordings from wild-type body-wall muscles revealed rhythmic bursts of spikes. In eag Sh mutants, this rhythmic activity was accompanied by or superimposed on periods of strong tonic activity. This abnormal pattern of activity could be partially suppressed by napts in combination with eag Sh.

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“…We expect, however, that the extracellular length constant is much shorter at parts of nerve terminal branches with small, isolated synaptic contacts (e.g. ChE rings), since the cleft between the muscle fibre and the Schwann cell is considerably larger outside the immediate synaptic contact (see below and Anzil et al 1984). Differences in the extracellular length constant should also arise from differences in the width of the synaptic gutter, which is bound to be different at terminal branches with different axon diameters (cf.…”

Section: Electrophy8iologymentioning

confidence: 99%

“…Evidence has been presented in previous investigations that the adult frog neuromuscular junction is not a static structure but continually undergoes some physiological remodelling (Wernig, P6cot-Dechavassine & St6ver, 1980a, b). In the preceding paper (Anzil, Bieser & Wernig, 1984), newly formed synaptic contacts were ascribed to sites which, in the light microscope appeared as small rings ofcholinesterase (ChE) reaction product. Here we report electrophysiological data on spontaneous transmitter release at different points along a single neuromuscular junction.…”

Section: Introductionmentioning

confidence: 99%

Different quantal responses within single frog neuromuscular junctions.

Bieser¹,

Wernig²,

Zucker³

1984

The Journal of Physiology

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SUMMARY1. At frog neuromuscular junctions spontaneous miniature end-plate potentials (m.e.p.p.s) were recorded from several isolated spots within single synapses. This was done by consecutively placing an extracellular glass micro-electrode (focal electrode) at different recording sites, while the intracellular electrode remained in one place.2. After each set of recordings, muscles were stained to reveal both axon terminals and cholinesterase (ChE) such that the exact position of each recording site could be determined.3. In many nerve terminal branches a similar quantum size was found at several different spots. In other instances, however, mean quantum amplitudes varied by 10-60 % at different spots along the same terminal branches.4. As a control, individual spots were recorded from repeatedly after repositioning the focal electrode. In these recordings mean m.e.p.p. amplitude varied by only 5-10 %.5. It is concluded that quantum size within a single junction is similar at many spots, but deviates markedly at others. Correlation of this variation with the stained preparations suggested that spots where quanta significantly larger or smaller than normal were recorded were either at ChE rings or at the distal ends of nerve branches, respectively; at different nerve terminal branches within the same junction, quantum amplitudes were similar in many cases but deviated in others.6. The results are consistent with ultrastructural evidence that frog neuromuscular junctions are non-homogeneous structures which undergo continual remodelling.

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Light and electron microscopic identification of nerve terminal sprouting and retraction in normal adult frog muscle.

Cited by 53 publications

References 17 publications

Terminal Schwann Cells Participate in Neuromuscular Synapse Remodeling during Reinnervation following Nerve Injury

Terminal Schwann Cells Participate in Neuromuscular Synapse Remodeling during Reinnervation following Nerve Injury

Morphological plasticity of motor axons in Drosophila mutants with altered excitability

Different quantal responses within single frog neuromuscular junctions.

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