Role of axoplasmic transport in neurotrophic regulation of muscle end plate acetylcholinesterase

Hl, Ferdandez; Inestrosa, N. C.

doi:10.1038/262055a0

Cited by 57 publications

(22 citation statements)

References 15 publications

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“…On the other hand, after myotubes were formed and 16 S AChE was synthesized, the specific activity of AChE decreased with the time in culture in the absence of neural influence. Denervated muscles show a similar decrease in AChE [1,3,14]. The decrease observed in vitro may reflect a mechanism by which innervating nerves regulate the AChE activity in muscles and its localization at synaptic regions.…”

Section: Discussionmentioning

confidence: 99%

Multiple forms of acetylcholinesterase in clonal muscle cells

Sugiyama

1977

FEBS Letters

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Section: Discussionmentioning

confidence: 99%

Multiple forms of acetylcholinesterase in clonal muscle cells

Sugiyama

1977

FEBS Letters

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“…This "overshoot" is prevented by the suppression of axoplasmic flow by applyingvinblastine to the motor nerve [ 5 31. Blockade of axoplasmic flow in the cat hypoglossal nerve decreases AChE activity in end-plateenriched segments of the genohyoid muscle by 50% after 10 days [54]. However, neither surgical denervation nor interference with axoplasmic flow has yet been shown to result in a total loss of end-plate AChE, and end-plate AChE can be detected histochemically even eight months after denervation [55].…”

Section: Discussionmentioning

confidence: 99%

A new myasthenic syndrome with end‐plate acetylcholinesterase deficiency, small nerve terminals, and reduced acetylcholine release

Engel

Lambert

Gómez

1977

Annals of Neurology

225

108

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A new myasthenic syndrome is described in a patient whose symptoms began soon after birth and included generalized weakness increased by exertion, easy fatigability, hyporeflexia, and refractoriness to anticholinesterase drugs. Electromyography showed a decremental response at all frequencies of stimulation and a repetitive response to single nerve stimulation. Miniature end-plate potentials (mepps) were of normal amplitude but of decreased frequency. The mepp duration and half-decay time were prolonged, and prostigmine was without any addtitional effect. The quantum content of the end-plate potential was decreased due to a reduced store of quanta immediately available for release, but the probability of release was normal. Quantitative electron microscopy demonstrated a 3-fold to 4-fold decrease of nerve terminal size and reduced postsynaptic membrane density. The postsynaptic folds showed focal degeneration, and many were distended by labyrinthine membranous networks that communicated with the synaptic space. Degenerating nuclei were found in the junctional sarcoplasm. The ultrastructural localization of the acetylcholine receptor protein was normal. Acetylcholinesterase (AChE) was absent from the motor end-plates by histochemical and electron cytochemical criteria. Biochemical studies indicated total absence of the end-plate-specific 16 S species of AChE and marked decrease in total muscle AChE. A congenital defect in the molecular assembly of AChE or in its attachment to the postsynaptic membrane might represent the basic abnormality and condition the morphological and physiological alterations.

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“…Thus, junctional AChE activity is reduced by colchicine applied locally to the nerve to block axonal transport (Fernandez & Inestrosa, 1976). Furthermore, a reduction in junctional AChE following nerve section occurs earlier with a short than with a long nerve stump .…”

Section: Discussionmentioning

confidence: 99%

Control of junctional acetylcholinesterase by neural and muscular influences in the rat.

Lømo¹,

Slater²

1980

The Journal of Physiology

134

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1. The development of AChE at ectopic neuromuscular junctions forming between a transplanted foreign nerve (the superficial fibular nerve) and the denervated soleus muscle has been studied in adult rats. 2. Junctional AChE activity began to appear in the vicinity of the fibular nerve sprouts 6‐7 days after section of the soleus nerve and 3‐4 days after the onset of transmission. 3. No histochemically detectable AChE appeared when the fibular nerve was cut 0‐4 days after the soleus nerve had been cut. 4. Direct electrical stimulation of the denervated soleus muscle caused plaques of true AChE, as determined by inhibitor studies, to appear in muscles where the fibular nerve had been cut 2‐4 days after the soleus nerve but not in muscles where the two nerves had been cut at the same time. The plaques appeared only in the vicinity of fibular nerve sprouts and coincided with newly formed but stable peaks of ACh sensitivity. Local application of Neostigmine prolonged and increased the depolarising response evoked by pulses of ACh at these sites. 5. In muscles where the fibular nerve was intact the AChE plaques changed gradually over a few weeks from an immature appearance to a mature appearance characteristic of normal end‐plates. In stimulated muscles where the fibular nerve had been cut the plaques stained intensely but remained morphologically immature. 6. We conclude (1) that muscle activity is important for the appearance of AChE at developing neuromuscular junctions and (2) that AChE accumulates only at sites on the muscle surface where the nerve fibres have left a ‘trace’ upon contact with the muscle fibres. These traces form quickly and persist after nerve‐muscle interaction of as little as 2 days. The muscle appears as a major source of junctional AChE since stimulation of the muscle induces intense AChE activity in muscles where the nerve has degenerated.

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Role of axoplasmic transport in neurotrophic regulation of muscle end plate acetylcholinesterase

Cited by 57 publications

References 15 publications

Multiple forms of acetylcholinesterase in clonal muscle cells

Multiple forms of acetylcholinesterase in clonal muscle cells

A new myasthenic syndrome with end‐plate acetylcholinesterase deficiency, small nerve terminals, and reduced acetylcholine release

Control of junctional acetylcholinesterase by neural and muscular influences in the rat.

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