ArticleCell reports2024
Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed.
- Chronic Diazepam Reveals Excessive Homeostatic Gain in SOD1International journal of molecular sciences · 2026Article
- Chronic diazepam reveals excessive homeostatic gain in SOD1bioRxiv : the preprint server for biology · 2026Article
- Spinal motoneuron excitability is homeostatically regulated through β-adrenergic neuromodulation in wild-type and presymptomatic SOD1 mice.Progress in neurobiology · 2026Article
- Machine-learning classification of motor unit types in the adult mouse.The Journal of physiology · 2026Article
- Article
- Spinal circuit mechanisms constrain therapeutic windows for ALS intervention: A computational modeling study.Neurobiology of disease · 2026Article
- Synaptopathy in the TDP-43ΔNLS Mouse Model of Sporadic Amyotrophic Lateral Sclerosis.The European journal of neuroscience · 2025Article
- Personalized mapping of inhibitory spinal cord circuits in humans via noninvasive neural decoding and in silico modeling.Science advances · 2025Article
- Episodic rhythmicity is generated by a distributed neural network in the developing mammalian spinal cord.iScience · 2025Article
- Excitatory to inhibitory synaptic ratios are unchanged at presymptomatic stages in multiple models of ALS.PloS one · 2024Article
- Augmented and prematurely occurring H-reflex recovery curve shows enhanced spinal network excitability in ALS patients when employing the double stimulation paradigm.Frontiers in neurologyArticle
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Abstract
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.
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