ArticleThe American journal of pathology2009
Glycinergic innervation of motoneurons is deficient in amyotrophic lateral sclerosis mice: a quantitative confocal analysis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Elucidating the Role of Cerebellar Synaptic Dysfunction in C9orf72-ALS/FTD - a Systematic Review and Meta-Analysis.Cerebellum (London, England) · 2022Pooled it
- Human iPSC-Derived Spinal Neurons Carrying the ALS FUS (P525L) Mutation Exhibit Lower Response to Inhibitory Neurotransmitters.Cellular and molecular neurobiology · 2026Article
- Multi-path direct current spinal stimulation extended survival in the SOD1-G93A model of amyotrophic lateral sclerosis.Frontiers in neurology · 2025Article
- Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.Cell reports · 2024Article
- Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.bioRxiv : the preprint server for biology · 2024Article
- Spinal inhibitory neurons degenerate before motor neurons and excitatory neurons in a mouse model of ALS.Science advances · 2024Article
- How do we get from hyperexcitability to excitotoxicity in amyotrophic lateral sclerosis?Brain : a journal of neurology · 2024Review
- Excitatory to inhibitory synaptic ratios are unchanged at presymptomatic stages in multiple models of ALS.PloS one · 2024Article
- Article
- Potential contribution of spinal interneurons to the etiopathogenesis of amyotrophic lateral sclerosis.Frontiers in neuroscience · 2024Review
- Proteasome localization and activity in pig brain andFrontiers in cellular neuroscience · 2024Article
- ENGRAILED-1 transcription factor has a paracrine neurotrophic activity on adult spinal α-motoneurons.EMBO reports · 2023Article
- Inhibitory interneurons show early dysfunction in a SOD1 mouse model of amyotrophic lateral sclerosis.The Journal of physiology · 2023Article
- Neural circuit and synaptic dysfunctions in ALS-FTD pathology.Frontiers in neural circuits · 2023Review
- Accumulation of misfolded SOD1 outlines distinct patterns of motor neuron pathology and death during disease progression in a SOD1Brain pathology (Zurich, Switzerland) · 2022Article
- Article
- The Cell Autonomous and Non-Cell Autonomous Aspects of Neuronal Vulnerability and Resilience in Amyotrophic Lateral Sclerosis.Biology · 2022Review
- Basal forebrain magnocellular cholinergic systems are damaged in mice following neonatal hypoxia-ischemia.The Journal of comparative neurology · 2022Article
- Proprioception revisited: where do we stand?Current opinion in physiology · 2021Article
- Article
5 more citing papers are in PubMed but not listed here.
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2 authors.
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Abstract
Altered motoneuron excitability is involved in amyotrophic lateral sclerosis pathobiology. To test the hypothesis that inhibitory interneuron innervation of spinal motoneurons is abnormal in an amyotrophic lateral sclerosis mouse model, we measured GABAergic, glycinergic, and cholinergic immunoreactive terminals on spinal motoneurons in mice expressing a mutant form of human superoxide dismutase-1 with a Gly93-->Ala substitution (G93A-SOD1) and in controls at different ages. Glutamic acid decarboxylase, glycine transporter-2, and choline acetyltransferase were used as markers for GABAergic, glycinergic, and cholinergic terminals, respectively. Triple immunofluorescent labeling of boutons contacting motoneurons was visualized by confocal microscopy and analyzed quantitatively. Glycine transporter-2-bouton density on lateral motoneurons was decreased significantly in G93A-SOD1 mice compared with controls. This reduction was absent at 6 weeks of age but present in asymptomatic 8-week-old mice and worsened with disease progression from 12 to 14 weeks of age. Motoneurons lost most glycinergic innervation by 16 weeks of age (end-stage) when there was a significant decrease in the numbers of motoneurons and choline acetyltransferase-positive boutons. No significant differences in glutamic acid decarboxylase-bouton densities were found in G93A-SOD1 mice. Reduction of glycinergic innervation preceded mitochondrial swelling and vacuolization. Calbindin-positive Renshaw cell number was decreased significantly at 12 weeks of age in G93A-SOD1 mice. Thus, either the selective loss of inhibitory glycinergic regulation of motoneuron function or glycinergic interneuron degeneration contributes to motoneuron degeneration in amyotrophic lateral sclerosis.
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