Acetylcholine release from motor-nerve endings in rats treated with neostigmine

Roberts, David; Thesleff, S.

doi:10.1016/0014-2999(69)90186-1

Cited by 35 publications

(21 citation statements)

References 5 publications

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“…On stimulation of the phrenic nerve with repetitive pulses at 100 Hz, no Wedensky inhibition, a typical phenomenon of cholinesterase inhibition, was observed, indicating that the action of neostigmine had disappeared. With similar treatment, Roberts & Thesleff (1969) also found that the enzyme activity was within normal. 615 Release of acetylcholine As shown in Table 1, the output of acetylcholine during 20 min stimulation at 100 Hz for 5 sec every 20 sec from normal hemidiaphragms was 27 ng ± 5*2 (S.D.)…”

Section: Resultsmentioning

confidence: 71%

“…It is interesting that chronic treatment with neostigmine also decreased the number of acetylcholine receptors. This may account for the decreased amplitude of miniature end-plate potentials found by Roberts & Thesleff (1969) in similarly treated rat muscles. It is apparent that the decrease of acetylcholine receptors may contribute to the muscle weakness in rats and the cholinergic crisis in myasthaenia gravis after chronic neostigmine treatment.…”

Section: Discussionmentioning

confidence: 90%

“…These two data together may indicate that the quantum size was not reduced. Since the total store of acetylcholine was not reduced, a change might have occurred in the small releasable pool of acetylcholine as pointed out by Roberts & Thesleff (1969) or in the release mechanism per se. It is interesting that chronic treatment with neostigmine also decreased the number of acetylcholine receptors.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown by Roberts & Thesleff (1969) that chronic treatment with neostigmine in rats caused muscle weakness and reduction of the quantal content of end-plate potentials. The release and content of acetylcholine were therefore also studied.…”

Section: Introductionmentioning

confidence: 99%

“…Neostigmine methylsulphate (0-1 mg) was administered subcutaneously twice daily for 7 days as previously described by Roberts & Thesleff (1969). Atropine sulphate (1 mg) was also given 30 min before injection of neostigmine in the first 2 days in order to minimize the muscarinic effect.…”

Section: Neostigmine Treatmentmentioning

confidence: 99%

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Influence of chronic neostigmine treatment on the number of acetylcholine receptors and the release of acetylcholine from the rat diaphragm

Chang¹,

Chen²,

Chuang³

1973

The Journal of Physiology

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SUMMARY1. Rats were treated twice daily for 7 days with neostigmine and the diaphragm was isolated for study of its acetylcholine content, release upon nerve stimulation and the number of receptors in the end-plate.2. While the content of total acetylcholine was unchanged, the release of acetylcholine on stimulation with trains of 500 pulses at 100 Hz every 20 sec was reduced by about 50 %. Five days after the end of neostigmine treatment the release of acetylcholine recovered to normal.3. The total number of acetylcholine receptors in the end-plate as measured from the binding of N, O-di[3H]acetyl z-bungarotoxin was reduced from 2-1 x 107 to 1-2 x 107 per end-plate. 4. The above-mentioned changes are not due to acute pharmacological effects of neostigmine, nor to an immediate effect of cholinesterase inhibition but presumably due to chronic accumulation of acetylcholine at the neuromuscular junction.

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Section: Resultsmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Neostigmine Treatmentmentioning

confidence: 99%

See 3 more Smart Citations

Influence of chronic neostigmine treatment on the number of acetylcholine receptors and the release of acetylcholine from the rat diaphragm

Chang¹,

Chen²,

Chuang³

1973

The Journal of Physiology

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Neostigmine Methylsulfate

Ward¹

1975

Arch Neurol

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Three groups of 200-gm rats were injected subcutaneously with neostigmine methylsulfate (1 mg/kg/day) for 7, 30, and 100 days. Electrophysiological changes were assessed in vitro, using microelectrode techniques to examine diaphragm muscles of treated and untreated animals. Miniature end-plate potential (MEPP) amplitude decreased in neostigmine-treated preparations. Guanidine hydrochloride enhances transmitter release and increases MEPP frequency in control preparations. Neostigmine-treated animals examined between 6 to 72 hours after discontinuation of neostigmine therapy showed impaired response to the facilitating influence of guanidine. Recovery of response to guanidine was inversely related to length of treatment with neostigmine. Results of electron-microscopic examination of motor end-plates in treated animals revealed ultrastructural changes, including simplified end-plates, and, occasionally, multiple, separate, junctional regions. Therefore, the chronic administration of cholinesterase inhibitors in man may have a deleterious effect, as well as a transient beneficial one.

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Prednisone‐neostigmine interactions at cholinergic junctions

et al. 1979

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The effect of corticosteroid (prednisone) and/or chronic anticholinesterase (neostigmine) treatment on alpha-bungarotoxin binding was examined in the diaphragms of male rats. In endplate regions of the diaphragm, prednisone treatment had no effect on the density of toxin binding sites, either when given alone or when administered in conjunction with neostigmine while neostigmine was observed to reduce specific binding to less than half after one week.

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Acetylcholine release from motor-nerve endings in rats treated with neostigmine

Cited by 35 publications

References 5 publications

Influence of chronic neostigmine treatment on the number of acetylcholine receptors and the release of acetylcholine from the rat diaphragm

Influence of chronic neostigmine treatment on the number of acetylcholine receptors and the release of acetylcholine from the rat diaphragm

Neostigmine Methylsulfate

Prednisone‐neostigmine interactions at cholinergic junctions

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