Relaxation of synaptic inhibitory events as a compensatory mechanism in fetal SOD spinal motor networks.
Amyotrophic Lateral Sclerosis
/ genetics
Animals
Chlorides
/ metabolism
Disease Models, Animal
Fetus
GABAergic Neurons
/ metabolism
Glycine
/ metabolism
Humans
Mice
Mice, Transgenic
Motor Neurons
/ metabolism
Neural Inhibition
/ genetics
Spinal Cord
/ metabolism
Superoxide Dismutase-1
/ genetics
Symporters
/ genetics
Synaptic Transmission
/ genetics
gamma-Aminobutyric Acid
/ genetics
K Cl- Cotransporters
ALS disease
GABA/glycine inhibition
SOD1G93A
modelling
mouse
neuroscience
patch-clamp
relaxation time course
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
23 12 2019
23 12 2019
Historique:
received:
27
08
2019
accepted:
20
12
2019
pubmed:
24
12
2019
medline:
13
6
2020
entrez:
24
12
2019
Statut:
epublish
Résumé
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease affecting motor neurons (MNs) during late adulthood. Here, with the aim of identifying early changes underpinning ALS neurodegeneration, we analyzed the GABAergic/glycinergic inputs to E17.5 fetal MNs from SOD1
Identifiants
pubmed: 31868588
doi: 10.7554/eLife.51402
pii: 51402
pmc: PMC6974356
doi:
pii:
Substances chimiques
Chlorides
0
Symporters
0
gamma-Aminobutyric Acid
56-12-2
Sod1 protein, mouse
EC 1.15.1.1
Superoxide Dismutase-1
EC 1.15.1.1
Glycine
TE7660XO1C
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2019, Branchereau et al.
Déclaration de conflit d'intérêts
PB, EM, WC, LS, FH, AL, UD, HZ, DC No competing interests declared
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