Publication:
Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression

dc.contributor.coauthorİsak, Barış
dc.contributor.departmentN/A
dc.contributor.kuauthorÖzyurt, Mustafa Görkem
dc.contributor.kuauthorTopkara, Betilay
dc.contributor.kuauthorTürker, Kemal Sıtkı
dc.contributor.kuprofilePhD Student
dc.contributor.kuprofilePhD Student
dc.contributor.kuprofileFaculty Member
dc.contributor.schoolcollegeinstituteGraduate School of Sciences and Engineering
dc.contributor.schoolcollegeinstituteGraduate School of Health Sciences
dc.contributor.schoolcollegeinstituteSchool of Medicine
dc.contributor.yokidN/A
dc.contributor.yokid353320
dc.contributor.yokid6741
dc.date.accessioned2024-11-09T23:05:20Z
dc.date.issued2020
dc.description.abstractObjectives: Amyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients. Methods: In two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects. Results: Compared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 +/- 2.6 ms) but not in nonlumbar-affected patients (29.7 +/- 12.4 ms, P < 0.0001) compared to controls (30.8 +/- 7.2 ms, P < 0.0001). Conclusion: The current study revealed that spinal inhibitory circuits are impaired in ALS. Significance: These findings may provide insight for proposing new therapeutic approaches and following disease progression in humans.
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue12
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsorshipKoc University School of Medicine
dc.description.sponsorshipMarmara University Research & Education Hospital
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUB_ITAK) nder the "2211-A National Scholarship Program for Ph.D. Students" We acknowledge the role of the Koc University School of Medicine and Marmara University Research & Education Hospital for funding this project. We also thank the Scientific and Technological Research Council of Turkey (TUB_ITAK) for funding Mustafa Gorkem Ozyurt under the ``2211-A National Scholarship Program for Ph.D. Students".
dc.description.volume131
dc.identifier.doi10.1016/j.clinph.2020.09.021
dc.identifier.eissn1872-8952
dc.identifier.issn1388-2457
dc.identifier.quartileQ2
dc.identifier.scopus2-s2.0-85094882495
dc.identifier.urihttp://dx.doi.org/10.1016/j.clinph.2020.09.021
dc.identifier.urihttps://hdl.handle.net/20.500.14288/8773
dc.identifier.wos595528200012
dc.keywordsRecurrent inhibition
dc.keywordsRenshaw cells
dc.keywordsAmyotrophic lateral sclerosis
dc.keywordsPost-activation depression
dc.keywordsMotoneuron als-linked SOD1
dc.keywordsSoleus h-reflex
dc.keywordsMotor units
dc.keywordsPostsynaptic potentials
dc.keywordsMotoneurons
dc.keywordsVulnerability
dc.keywordsCotransporter
dc.keywordsHomeostasis
dc.keywordsFrequency
dc.keywordsDischarge
dc.languageEnglish
dc.publisherElsevier Ireland Ltd
dc.sourceClinical Neurophysiology
dc.subjectClinical neurology
dc.subjectNeurosciences
dc.titleAmyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.authorid0000-0003-2531-1174
local.contributor.authorid0000-0002-3509-9296
local.contributor.authorid0000-0001-9962-075X
local.contributor.kuauthorÖzyurt, Mustafa Görkem
local.contributor.kuauthorTopkara, Betilay
local.contributor.kuauthorTürker, Kemal Sıtkı

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