Home > Publications Database > Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration. > print

001     273977
005     20250127091351.0
024 7 _ |a 10.1016/j.celrep.2024.115046
|2 doi
024 7 _ |a pmid:39656589
|2 pmid
024 7 _ |a 2211-1247
|2 ISSN
024 7 _ |a 2639-1856
|2 ISSN
024 7 _ |a altmetric:171841298
|2 altmetric
037 _ _ |a DZNE-2024-01426
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Nascimento, Filipe
|b 0
245 _ _ |a Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.
260 _ _ |a [New York, NY]
|c 2024
|b Elsevier
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1734339391_1124
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a In many neurological conditions, early-stage neural circuit adaptation preserves relatively normal behavior. In some diseases, spinal motoneurons progressively degenerate yet movement remains initially preserved. This study investigates whether these neurons and associated microcircuits adapt in a mouse model of progressive motoneuron degeneration. Using a combination of in vitro and in vivo electrophysiology and super-resolution microscopy, we find that, early in the disease, neurotransmission in a key pre-motor circuit, the recurrent inhibition mediated by Renshaw cells, is reduced by half due to impaired quantal size associated with decreased glycine receptor density. This impairment is specific and not a widespread feature of spinal inhibitory circuits. Furthermore, it recovers at later stages of disease. Additionally, an increased probability of release from proprioceptive afferents leads to increased monosynaptic excitation of motoneurons. We reveal that, in this motoneuron degenerative condition, spinal microcircuits undergo specific multiphasic homeostatic compensations that may contribute to preservation of force output.
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a ALS
|2 Other
650 _ 7 |a CP: Cell biology
|2 Other
650 _ 7 |a CP: Neuroscience
|2 Other
650 _ 7 |a Renshaw cells
|2 Other
650 _ 7 |a electrophysiology
|2 Other
650 _ 7 |a glycine receptors
|2 Other
650 _ 7 |a motoneurons
|2 Other
650 _ 7 |a motor control
|2 Other
650 _ 7 |a quantal analysis
|2 Other
650 _ 7 |a sensory afferents
|2 Other
650 _ 7 |a spinal cord
|2 Other
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Motor Neurons: metabolism
|2 MeSH
650 _ 2 |a Motor Neurons: pathology
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Homeostasis
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Spinal Cord: pathology
|2 MeSH
650 _ 2 |a Spinal Cord: metabolism
|2 MeSH
650 _ 2 |a Synaptic Transmission: physiology
|2 MeSH
650 _ 2 |a Receptors, Glycine: metabolism
|2 MeSH
650 _ 2 |a Nerve Degeneration: pathology
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Renshaw Cells: metabolism
|2 MeSH
700 1 _ |a Özyurt, M Görkem
|b 1
700 1 _ |a Halablab, Kareen
|0 P:(DE-2719)9001676
|b 2
|u dzne
700 1 _ |a Bhumbra, Gardave Singh
|b 3
700 1 _ |a Caron, Guillaume
|b 4
700 1 _ |a Bączyk, Marcin
|b 5
700 1 _ |a Zytnicki, Daniel
|b 6
700 1 _ |a Manuel, Marin
|b 7
700 1 _ |a Roselli, Francesco
|0 P:(DE-2719)2812851
|b 8
|u dzne
700 1 _ |a Brownstone, Rob
|b 9
700 1 _ |a Beato, Marco
|b 10
773 _ _ |a 10.1016/j.celrep.2024.115046
|g Vol. 43, no. 12, p. 115046 -
|0 PERI:(DE-600)2649101-1
|n 12
|p 115046
|t Cell reports
|v 43
|y 2024
|x 2211-1247
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/273977/files/DZNE-2024-01426.pdf
856 4 _ |y OpenAccess
|x pdfa
|u https://pub.dzne.de/record/273977/files/DZNE-2024-01426.pdf?subformat=pdfa
909 C O |o oai:pub.dzne.de:273977
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 2
|6 P:(DE-2719)9001676
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 8
|6 P:(DE-2719)2812851
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 0
914 1 _ |y 2024
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2023-10-26
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2023-10-26
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2023-10-26
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2023-10-26
915 _ _ |a Creative Commons Attribution CC BY 4.0
|0 LIC:(DE-HGF)CCBY4
|2 HGFVOC
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b CELL REP : 2022
|d 2023-10-26
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2023-05-02T08:49:39Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2023-05-02T08:49:39Z
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2023-10-26
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2023-10-26
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2023-10-26
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b DOAJ : Anonymous peer review
|d 2023-05-02T08:49:39Z
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2023-10-26
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b CELL REP : 2022
|d 2023-10-26
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2023-10-26
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2023-10-26
920 1 _ |0 I:(DE-2719)1910001
|k AG Roselli
|l Metabolic Changes in Neurodegeneration
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1910001
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21