| Altered developmental changes of neuromuscular junction in hypo- and hyperthyroid rats. | |
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MedLine Citation:
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PMID: 6128407 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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1. Effects of thyroid hormone on the development of neuromuscular junctions (n.m.j.s.) were investigated electrophysiologically in the diaphragms (sternal region) of normal, hypo- and hyperthyroid rats from the age of birth (day 0) to day 35.2. Hypothyroidism in new-born rats was induced either by daily administration of propylthiouracil to mothers or by subcutaneous injection of 150 muCi (131)I on day 1. Hyperthyroidism was induced by daily injection of thyroxine.3. In normal rats up to day 10, muscle fibres were innervated polyneuronally. By day 20, multiple innervation was eliminated and muscle fibres received only a single input. In hypothyroid rats elimination of polyneuronal innervation was retarded by 5-8 days, while in hyperthyroid rats the elimination was accelerated by 2-3 days.4. The frequency of miniature end-plate potentials (m.e.p.p.s) in normal rats increased from one per 40 sec on days 0-5 to 1/sec on days 25-35. The m.e.p.p. frequency in hypothyroid rats was 25-65% of that in normal rats of the same age. In hyperthyroid rats the m.e.p.p. frequency was normal up to day 18 but subnormal afterwards. The duration of m.e.p.p. measured on day 22-23 was slower in hypothyroid rats and faster in hyperthyroid rats, relative to m.e.p.ps in normal rats.5. The sensitivity to acetylcholine (ACh) at extrajunctional regions in normal rats was about 100 mV/nC at birth and declined to 1 mV/nC by day 26. In hypothyroid rats, the ACh sensitivity was as high as 30 mV/nC on day 26; in hyperthyroid rats, ACh sensitivity on day 26 was undetectable.6. With pairs of nerve stimuli (applied at a 50 msec interval), the second end-plate potential was facilitated until day 10 and depressed after day 16 in normal rats. This shift from facilitation to depression during development was not altered in either hypo-or hyperthyroid rats.7. It is concluded that the lack and excess of thyroid hormone retards and facilitates the development of n.m.j.s. respectively. Possible mechanisms for this altered development are discussed. |
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Authors:
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K Kawa; K Obata |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The Journal of physiology Volume: 329 ISSN: 0022-3751 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 1982 Aug |
Date Detail:
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Created Date: 1983-01-07 Completed Date: 1983-01-07 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 143-61 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Action Potentials Aging Animals Body Weight Female Hyperthyroidism / physiopathology* Hypothyroidism / physiopathology* Male Neuromuscular Junction / drug effects, physiopathology* Neurotransmitter Agents / secretion Phrenic Nerve / physiopathology Rats Rats, Inbred Strains Respiration |
| Chemical | |
Reg. No./Substance:
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0/Neurotransmitter Agents; 51-84-3/Acetylcholine |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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