ArticleAmerican journal of physiology. Endocrinology and metabolism2012
Acetylcholinesterase deficiency contributes to neuromuscular junction dysfunction in type 1 diabetic neuropathy.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 27 citations in OpenAlex.
- Characterization of sensory and motor dysfunction and morphological alterations in late stages of type 2 diabetic mice.Frontiers in endocrinology · 2024Article
- Splicing regulation of GFPT1 muscle-specific isoform and its roles in glucose metabolisms and neuromuscular junction.iScience · 2023Article
- Towards the Preparation of a Hydrogel from Lyophilisates of thePharmaceutics · 2022Article
- Cholinesterases in Tripartite Neuromuscular Synapse.Frontiers in molecular neuroscience · 2021Review
- Reaching task performance is associated to neuromuscular junction adaptations in rats with induced diabetes mellitus.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Acupotomy Alleviates Energy Crisis at Rat Myofascial Trigger Points.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Article
- Age-dependent modulation of fasting and long-term dietary restriction on acetylcholinesterase in non-neuronal tissues of mice.Molecular and cellular biochemistry · 2016Article
- Effect of streptozotocin-induced diabetes on performance on a progressive ratio schedule.Psychopharmacology · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Diabetic neuropathy is associated with functional and morphological changes of the neuromuscular junction (NMJ) associated with muscle weakness. This study examines the effect of type 1 diabetes on NMJ function. Swiss Webster mice were made diabetic with three interdaily ip injections of streptozotocin (STZ). Mice were severely hyperglycemic within 7 days after the STZ treatment began. Whereas performance of mice on a rotating rod remained normal, the twitch tension response of the isolated extensor digitorum longus to nerve stimulation was reduced significantly at 4 wk after the onset of STZ-induced hyperglycemia. This mechanical alteration was associated with increased amplitude and prolonged duration of miniature end-plate currents (mEPCs). Prolongation of mEPCs was not due to expression of the embryonic acetylcholine receptor but to reduced muscle expression of acetylcholine esterase (AChE). Greater sensitivity of mEPC decay time to the selective butyrylcholinesterase (BChE) inhibitor PEC suggests that muscle attempts to compensate for reduced AChE levels by increasing expression of BChE. These alterations of AChE are attributed to STZ-induced hyperglycemia since similar mEPC prolongation and reduced AChE expression were found for db/db mice. The reduction of muscle end-plate AChE activity early during the onset of STZ-induced hyperglycemia may contribute to endplate pathology and subsequent muscle weakness during diabetes.
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