Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/3689
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dc.contributor.authorJara, Javier H.en_US
dc.contributor.authorSheets, Patrick L.en_US
dc.contributor.authorNigro, Maximiliano Joséen_US
dc.contributor.authorPerić, Minaen_US
dc.contributor.authorBrooks, Carolynen_US
dc.contributor.authorHeller, Daniel B.en_US
dc.contributor.authorMartina, Marcoen_US
dc.contributor.authorAndjus, Pavle R.en_US
dc.contributor.authorOzdinler, P. Handeen_US
dc.date.accessioned2020-11-26T15:52:59Z-
dc.date.available2020-11-26T15:52:59Z-
dc.date.issued2020-05-19-
dc.identifier.citationJara JH, Sheets PL, Nigro MJ, Perić M, Brooks C, Heller DB, Martina M, Andjus PR, Ozdinler PH. The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS. Front Mol Neurosci. 2020 May 19;13:73. doi: 10.3389/fnmol.2020.00073. PMID: 32508590; PMCID: PMC7248374.en_US
dc.identifier.issn1662-5099-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/3689-
dc.description.abstractThe brain is complex and heterogeneous. Even though numerous independent studies indicate cortical hyperexcitability as a potential contributor to amyotrophic lateral sclerosis (ALS) pathology, the mechanisms that are responsible for upper motor neuron (UMN) vulnerability remain elusive. To reveal the electrophysiological determinants of corticospinal motor neuron (CSMN, a.k.a UMN in mice) vulnerability, we investigated the motor cortex of hSOD1G93A mice at P30 (postnatal day 30), a presymptomatic time point. Glutamate uncaging by laser scanning photostimulation (LSPS) revealed altered dynamics especially within the inhibitory circuitry and more specifically in L2/3 of the motor cortex, whereas the excitatory microcircuits were unchanged. Observed microcircuitry changes were specific to CSMN in the motor column. Electrophysiological evaluation of the intrinsic properties in response to the microcircuit changes, as well as the exon microarray expression profiles of CSMN isolated from hSOD1G93A and healthy mice at P30, revealed the presence of a very dynamic set of events, ultimately directed to establish, maintain and retain the balance at this early stage. Also, the expression profile of key voltage-gated potassium and sodium channel subunits as well as of the inhibitory GABA receptor subunits and modulatory proteins began to suggest the challenges CSMN face at this early age. Since neurodegeneration is initiated when neurons can no longer maintain balance, the complex cellular events that occur at this critical time point help reveal how CSMN try to cope with the challenges of disease manifestation. This information is critically important for the proper modulation of UMNs and for developing effective treatment strategies.en_US
dc.relation.ispartofFrontiers in Molecular Neuroscienceen_US
dc.subjectamyotrophic lateral sclerosisen_US
dc.subjectcorticospinal motor neuronsen_US
dc.subjecthereditary spastic paraplegiaen_US
dc.subjectmicrocircuiten_US
dc.subjectneuronal vulnerabilityen_US
dc.subjectprimary lateral sclerosisen_US
dc.subjectupper motor neuronsen_US
dc.titleThe Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALSen_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fnmol.2020.00073-
dc.identifier.pmid32508590-
dc.description.rankM21-
dc.description.impact5.760-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptChair of General Physiology and Biophysics-
crisitem.author.deptChair of General Physiology and Biophysics-
crisitem.author.orcid0000-0002-8468-8513-
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