The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Increased extrajunctional acetylcholine sensitivity produced by chronic acetylcholine sensitivity produced by chronic post‐synaptic neuromuscular blockade.
Open accessAbstract
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
A study of supersensitivity in denervated mammalian skeletal muscle
Axelsson, J., & Thesleff, S. (1959) · The Journal of Physiology · doi:10.1113/jphysiol.1959.sp006233 · Cited by 732
The acetylcholine sensitivity of frog muscle fibres after complete or partial denervation
Miledi, R. (1960) · The Journal of Physiology · doi:10.1113/jphysiol.1960.sp006416 · Cited by 538
Control of ACh sensitivity by muscle activity in the rat
Lømo, T., & Rosenthal, J. (1972) · The Journal of Physiology · doi:10.1113/jphysiol.1972.sp009764 · Cited by 533
Hall, Z. W. (1973) · Journal of Neurobiology · doi:10.1002/neu.480040404 · Cited by 508
Self-citationOn the factors which determine the amplitude of the ‘miniature end‐plate potential’
Katz, B., & Thesleff, S. (1957) · The Journal of Physiology · doi:10.1113/jphysiol.1957.sp005811 · Cited by 468
Acetylcholine Receptors in Muscle Fibres
Miledi, R., & Potter, L. T. (1971) · Nature · doi:10.1038/233599a0 · Cited by 443
A study of foetal and new‐born rat muscle fibres
Diamond, J. M., & Miledi, R. (1962) · The Journal of Physiology · doi:10.1113/jphysiol.1962.sp006941 · Cited by 411
Supersensitivity of skeletal muscle produced by botulinum toxin
Thesleff, S. (1960) · The Journal of Physiology · doi:10.1113/jphysiol.1960.sp006463 · Cited by 322
Hartzell, H. C., & Fambrough, D. M. (1972) · The Journal of General Physiology · doi:10.1085/jgp.60.3.248 · Cited by 290
Binding of α-Bungarotoxin to Acetylcholine Receptors In Mammalian Muscle
Berg, D. K., Kelly, R. B., Sargent, P. B., Williamson, P., & Hall, Z. W. (1972) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.69.1.147 · Cited by 287
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Homeostatic plasticity in the developing nervous system
Turrigiano, G. G., & Nelson, S. B. (2004) · Nature Reviews Neuroscience · doi:10.1038/nrn1327 · Cited by 2,485
Activity-dependent scaling of quantal amplitude in neocortical neurons
Turrigiano, G. G., Leslie, K. R., Desai, N. S., Rutherford, L. C., & Nelson, S. B. (1998) · Nature · doi:10.1038/36103 · Cited by 2,226
Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function
Turrigiano, G. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a005736 · Cited by 1,139
Synaptic structure and development: The neuromuscular junction
Hall, Z. W., & Sanes, J. R. (1993) · Cell · doi:10.1016/s0092-8674(05)80031-5 · Cited by 834
Self-citationNerve‐induced and spontaneous redistribution of acetylcholine receptors on cultured muscle cells.
Anderson, M. J., & Cohen, M. W. (1977) · The Journal of Physiology · doi:10.1113/jphysiol.1977.sp011880 · Cited by 460
Metadata
- 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
- 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
- green
- www.ncbi.nlm.nih.gov
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review