ArticleAnesthesiology2014
Immobilization with atrophy induces de novo expression of neuronal nicotinic α7 acetylcholine receptors in muscle contributing to neurotransmission.
Article in Anesthesiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Acute tolerance to rocuronium -A case report.Anesthesia and pain medicine · 2024Article
- Effect of protracted dexamethasone exposure and its withdrawal on rocuronium-induced neuromuscular blockade and sugammadex reversal: an ex vivo rat study.Scientific reports · 2019Article
- Disruption of Neutrophil Extracellular Traps (NETs) Links Mechanical Strain to Post-traumatic Inflammation.Frontiers in immunology · 2019Article
- Effects of neuromuscular presynaptic muscarinic MClinical and experimental pharmacology & physiology · 2018Article
- GTS-21 attenuates loss of body mass, muscle mass, and function in rats having systemic inflammation with and without disuse atrophy.Pflugers Archiv : European journal of physiology · 2018Article
- Factors that affect the onset of action of non-depolarizing neuromuscular blocking agents.Korean journal of anesthesiology · 2017Review
- Differences in pharmacodynamic responses to rocuronium in normal or injured orbicularis oris are associated with expression of acetylcholine receptor subunits.Scientific reports · 2017Article
- Acute and perioperative care of the burn-injured patient.Anesthesiology · 2015Review
- Schwann cells sense and control acetylcholine spillover at the neuromuscular junction by α7 nicotinic receptors and butyrylcholinesterase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Neuronal involvement in muscular atrophy.Frontiers in cellular neuroscience · 2014Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundMature acetylcholine receptor (AChR) isoform normally mediates muscle contraction. The hypothesis that α7AChRs up-regulate during immobilization and contribute to neurotransmission was tested pharmacologically using specific blockers to mature (waglerin-1), immature (αA-OIVA), and α7AChRs (methyllycaconitine), and nonspecific muscle AChR antagonist, α-bungarotoxin.
methodsMice were immobilized; contralateral limbs were controls. Fourteen days later, anesthetized mice were mechanically ventilated. Nerve-stimulated tibialis muscle contractions on both sides were recorded, and blockers enumerated above sequentially administered via jugular vein. Data are mean ± standard error.
resultsImmobilization (N = 7) induced tibialis muscle atrophy (40.6 ± 2.8 vs. 52.1 ± 2.0 mg; P < 0.01) and decrease of twitch tension (34.8 ± 1.1 vs. 42.9 ± 1.5 g; P < 0.01). Waglerin-1 (0.3 ± 0.05 μg/g) significantly (P = 0.001; N = 9) depressed twitch tension on contralateral (≥97%) versus immobilized side (approximately 45%). Additional waglerin-1 (total dose 1.06 ± 0.12 μg/g or approximately 15.0 × ED50 in normals) could not depress twitch of 80% or greater on immobilized side. Immature AChR blocker, αA-OIVA (17.0 ± 0.25 μg/g) did not change tension bilaterally. Administration of α-bungarotoxin (N = 4) or methyllycaconitine (N = 3) caused 96% or greater suppression of the remaining twitch tension on immobilized side. Methyllycaconitine, administered first (N = 3), caused equipotent inhibition by waglerin-1 on both sides. Protein expression of α7AChRs was significantly (N = 3; P < 0.01) increased on the immobilized side.
conclusionsIneffectiveness of waglerin-1 suggests that the twitch tension during immobilization is maintained by receptors other than mature AChRs. Because αA-OIVA caused no neuromuscular changes, it can be concluded that immature AChRs contribute minimally to neurotransmission. During immobilization approximately 20% of twitch tension is maintained by up-regulation of α-bungarotoxin- and methyllycaconitine-sensitive α7AChRs.
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