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Cited by 159Nicotinic Acetylcholine Receptors StudyAnesthesia and Sedative AgentsMuscle Physiology and Disorders

Increased extrajunctional acetylcholine sensitivity produced by chronic acetylcholine sensitivity produced by chronic post‐synaptic neuromuscular blockade.

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Berg, D K, Hall, Z W·1975·The Journal of Physiology
DOI 10.1113/jphysiol.1975.sp010818PMC PMC1330828
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Abstract

1. Anaesthetized rats were paralysed for periods of up to 3 days by chronic administration of D‐tubocurarine (DTC), succinylcholine or alpha‐bungarotoxin. 2. After 3 days of treatment with DTC, the phrenic nerve remained active. Neuromuscular transmission and spontaneous miniature end‐plate potentials (m.e.p.p.s) were restored after removal of the DTC. Resting potentials and input resistances of muscle fibres that had been paralysed for 3 days were similar to those in denervated fibers. 3. Chronic neuromuscular blockade increased the binding of [125‐I]‐alpha‐bungarotoxin by extrajunctional regions of muscle. The time course of the increase was similar to that seen after denervation. Binding to muscles from animals that were anaesthetized and respirated, but not paralysed, was not increased. 4. Three days of paralysis increased the sensitivity of the extrajunctional muscle membrane to acetylcholine (ACh) applied by iontophoresis. 5. Approximately the same proportion of muscle fibres from muscles paralysed for 3 days gave overshooting action potentials in the presence of tetrodotoxin 10‐minus 6 g/ml. as did fibres form muscles denervated for 3 days. 6. Chronic paralysis did not change the accumulation of acetylcholinesterase above a ligation in the sciatic nerve. 7. These results are consistent with the idea that extrajunctional ACh sensitivity is normally controlled by muscle activity.

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  • Loss of synaptic innervation initiates an increase in muscle excitability through changes in postsynaptic receptor number and localization.

    “where it was observed that loss of synaptic innervation initiated an increase in muscle excitability through changes in postsynaptic receptor number and localization.”

    From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Berg and Hall, 1975

    The Abstract reports that chronic neuromuscular blockade increased extrajunctional acetylcholine-receptor binding and sensitivity in rat muscle, with changes similar to those after denervation. But the nerve remained active during blockade, so the paper does not establish that loss of synaptic innervation initiated the change or that receptor changes caused increased muscle excitability. (LLM, conf=0.84)

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Authors
Berg, D. K., & Hall, Z. W.
Venue
The Journal of Physiology
Publisher
Wiley
Published
1975-01
Volume
244
Issue
3
Pages
659-676
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.1975.sp010818
PMC
PMC1330828
OpenAlex
W2086218486
Cited by
159
References
43
Citations by year
2025: 1 · 2022: 2 · 2019: 2 · 2018: 2 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 1
FWCI
7.22
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Anesthesiology and Pain Medicine › Anesthesia and Sedative Agents
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
neuromuscular blockade, chronic paralysis, tubocurarine, succinylcholine, alpha-bungarotoxin, denervation, miniature end-plate potentials, phrenic nerve, muscle activity, acetylcholinesterase, neuromuscular transmission, tetrodotoxin
MeSH terms
Acetylcholine, Acetylcholinesterase, Action Potentials, Animals, Axons, Bungarotoxins, Iodine Isotopes, Iontophoresis, Male, Muscle Denervation, Synaptic Transmission, Neuromuscular Blocking Agents, Neuromuscular Junction, Phrenic Nerve, Receptors, Cholinergic, Succinylcholine, Tetrodotoxin, Tubocurarine, Rats

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