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Relaxation of synaptic inhibitory events as a compensatory mechanism in fetal SOD spinal motor networks
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Relaxation of synaptic inhibitory events as a compensatory mechanism in fetal SOD spinal motor networks
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Journal Article
Relaxation of synaptic inhibitory events as a compensatory mechanism in fetal SOD spinal motor networks
2019
Overview
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 G93A (SOD) mice in parallel with chloride homeostasis. Our results show that IPSCs are less frequent in SOD animals in accordance with a reduction of synaptic VIAAT-positive terminals. SOD MNs exhibited an E GABAAR 10 mV more depolarized than in WT MNs associated with a KCC2 reduction. Interestingly, SOD GABAergic/glycinergic IPSCs and evoked GABA A R-currents exhibited a slower decay correlated to elevated [Cl - ] i . Computer simulations revealed that a slower relaxation of synaptic inhibitory events acts as compensatory mechanism to strengthen GABA/glycine inhibition when E GABAAR is more depolarized. How such mechanisms evolve during pathophysiological processes remain to be determined, but our data indicate that at least SOD1 familial ALS may be considered as a neurodevelopmental disease.
Publisher
eLife Science Publications, Ltd,eLife Sciences Publications Ltd,eLife Sciences Publication,eLife Sciences Publications, Ltd
Subject
/ Amyotrophic lateral sclerosis
/ Amyotrophic Lateral Sclerosis - genetics
/ Amyotrophic Lateral Sclerosis - metabolism
/ Amyotrophic Lateral Sclerosis - pathology
/ Analysis
/ Animals
/ Chloride
/ Disease
/ Fetus
/ Fetuses
/ GABAergic Neurons - metabolism
/ GABAergic Neurons - pathology
/ gamma-Aminobutyric Acid - genetics
/ gamma-Aminobutyric Acid - metabolism
/ Glycine
/ Humans
/ Inhibitory postsynaptic potentials
/ Mice
/ Mutation
/ Neural Inhibition - genetics
/ Neurodevelopmental disorders
/ Neurons
/ Potassium-chloride cotransporter
/ SOD1G93A
/ Superoxide Dismutase-1 - genetics
