Journal Article

DZNE-2024-01426

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Spinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.

Nascimento, F. ; Özyurt, M. G. ; Halablab, K.DZNE* ; Bhumbra, G. S. ; Caron, G. ; Bączyk, M. ; Zytnicki, D. ; Manuel, M. ; Roselli, F.DZNE* ; Brownstone, R. ; Beato, M.

2024
Elsevier [New York, NY]

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Please use a persistent id in citations: doi:10.1016/j.celrep.2024.115046

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.

Keyword(s): Animals (MeSH) ; Motor Neurons: metabolism (MeSH) ; Motor Neurons: pathology (MeSH) ; Mice (MeSH) ; Homeostasis (MeSH) ; Disease Models, Animal (MeSH) ; Spinal Cord: pathology (MeSH) ; Spinal Cord: metabolism (MeSH) ; Synaptic Transmission: physiology (MeSH) ; Receptors, Glycine: metabolism (MeSH) ; Nerve Degeneration: pathology (MeSH) ; Mice, Inbred C57BL (MeSH) ; Renshaw Cells: metabolism (MeSH) ; ALS ; CP: Cell biology ; CP: Neuroscience ; Renshaw cells ; electrophysiology ; glycine receptors ; motoneurons ; motor control ; quantal analysis ; sensory afferents ; spinal cord

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Contributing Institute(s):

1. Metabolic Changes in Neurodegeneration (AG Roselli)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)

Appears in the scientific report 2024

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