{"title":"ELECTROPHYSIOLOGICAL STUDY OF THE LONG-TERM HYPOANDROGENISM EFFECT ON THE NEUROMUSCULAR APPARATUS","authors":"S. S. Tkachenko, O. G. Rodinsky","doi":"10.29254/2077-4214-2023-2-169-478-482","DOIUrl":null,"url":null,"abstract":"t-test). Changes in indi - cators were considered probable at p<0.05 [6]. The aim of the research was to find out the effect of long term androgen deficiency on skeletal muscles and neuromuscular synapse by bioelectrical activity studying. A 4-month hypoandrogenic state model was created by bilateral orchiectomy on sexually mature male Wistar rats. The parameters of the excitability, evoked potentials of the skeletal muscle and functional mobility of the neuromuscular synapse were studied. As a result, after 4 months of a hypoandrogenic state, the threshold of the neuromuscular apparatus excitation increased, especially with indirect irritation (up to 300%). The latency and duration of the evoked response, as well as the amplitude of the muscle action potential, were increased. A lengthening of the refractory period manifested itself in the slowing down of the response amplitude recovery to the test stimulus in the experimental group when stimulation with double pulses was used. During stimulation by series of impulses with a frequency more than 200 Hz, a rhythm transformation was observed in castrated animals, while in the control group the synapse was able to transmit a signal with a frequency up to 400 Hz. Thus, negative functional changes in the neuromuscular complex in conditions of long-term hypoandrogenemia can be explained mostly by bioelectrical changes of nervous structures of the neuromotor unit, namely, sharp decrease excitability, deterioration of the amplitude-time characteristics of the action potential and a decrease in the functional stability of the synaptic connection.","PeriodicalId":9360,"journal":{"name":"Bulletin of Problems Biology and Medicine","volume":"45 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bulletin of Problems Biology and Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.29254/2077-4214-2023-2-169-478-482","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
t-test). Changes in indi - cators were considered probable at p<0.05 [6]. The aim of the research was to find out the effect of long term androgen deficiency on skeletal muscles and neuromuscular synapse by bioelectrical activity studying. A 4-month hypoandrogenic state model was created by bilateral orchiectomy on sexually mature male Wistar rats. The parameters of the excitability, evoked potentials of the skeletal muscle and functional mobility of the neuromuscular synapse were studied. As a result, after 4 months of a hypoandrogenic state, the threshold of the neuromuscular apparatus excitation increased, especially with indirect irritation (up to 300%). The latency and duration of the evoked response, as well as the amplitude of the muscle action potential, were increased. A lengthening of the refractory period manifested itself in the slowing down of the response amplitude recovery to the test stimulus in the experimental group when stimulation with double pulses was used. During stimulation by series of impulses with a frequency more than 200 Hz, a rhythm transformation was observed in castrated animals, while in the control group the synapse was able to transmit a signal with a frequency up to 400 Hz. Thus, negative functional changes in the neuromuscular complex in conditions of long-term hypoandrogenemia can be explained mostly by bioelectrical changes of nervous structures of the neuromotor unit, namely, sharp decrease excitability, deterioration of the amplitude-time characteristics of the action potential and a decrease in the functional stability of the synaptic connection.