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000273977 037__ $$aDZNE-2024-01426
000273977 041__ $$aEnglish
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000273977 1001_ $$aNascimento, Filipe$$b0
000273977 245__ $$aSpinal microcircuits go through multiphasic homeostatic compensations in a mouse model of motoneuron degeneration.
000273977 260__ $$a[New York, NY]$$bElsevier$$c2024
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000273977 520__ $$aIn many neurological conditions, early-stage neural circuit adaptation preserves relatively normal behavior. In some diseases, spinal motoneurons progressively degenerate yet movement remains initially preserved. This study investigates whether these neurons and associated microcircuits adapt in a mouse model of progressive motoneuron degeneration. Using a combination of in vitro and in vivo electrophysiology and super-resolution microscopy, we find that, early in the disease, neurotransmission in a key pre-motor circuit, the recurrent inhibition mediated by Renshaw cells, is reduced by half due to impaired quantal size associated with decreased glycine receptor density. This impairment is specific and not a widespread feature of spinal inhibitory circuits. Furthermore, it recovers at later stages of disease. Additionally, an increased probability of release from proprioceptive afferents leads to increased monosynaptic excitation of motoneurons. We reveal that, in this motoneuron degenerative condition, spinal microcircuits undergo specific multiphasic homeostatic compensations that may contribute to preservation of force output.
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000273977 650_7 $$2Other$$aALS
000273977 650_7 $$2Other$$aCP: Cell biology
000273977 650_7 $$2Other$$aCP: Neuroscience
000273977 650_7 $$2Other$$aRenshaw cells
000273977 650_7 $$2Other$$aelectrophysiology
000273977 650_7 $$2Other$$aglycine receptors
000273977 650_7 $$2Other$$amotoneurons
000273977 650_7 $$2Other$$amotor control
000273977 650_7 $$2Other$$aquantal analysis
000273977 650_7 $$2Other$$asensory afferents
000273977 650_7 $$2Other$$aspinal cord
000273977 650_2 $$2MeSH$$aAnimals
000273977 650_2 $$2MeSH$$aMotor Neurons: metabolism
000273977 650_2 $$2MeSH$$aMotor Neurons: pathology
000273977 650_2 $$2MeSH$$aMice
000273977 650_2 $$2MeSH$$aHomeostasis
000273977 650_2 $$2MeSH$$aDisease Models, Animal
000273977 650_2 $$2MeSH$$aSpinal Cord: pathology
000273977 650_2 $$2MeSH$$aSpinal Cord: metabolism
000273977 650_2 $$2MeSH$$aSynaptic Transmission: physiology
000273977 650_2 $$2MeSH$$aReceptors, Glycine: metabolism
000273977 650_2 $$2MeSH$$aNerve Degeneration: pathology
000273977 650_2 $$2MeSH$$aMice, Inbred C57BL
000273977 650_2 $$2MeSH$$aRenshaw Cells: metabolism
000273977 7001_ $$aÖzyurt, M Görkem$$b1
000273977 7001_ $$0P:(DE-2719)9001676$$aHalablab, Kareen$$b2$$udzne
000273977 7001_ $$aBhumbra, Gardave Singh$$b3
000273977 7001_ $$aCaron, Guillaume$$b4
000273977 7001_ $$aBączyk, Marcin$$b5
000273977 7001_ $$aZytnicki, Daniel$$b6
000273977 7001_ $$aManuel, Marin$$b7
000273977 7001_ $$0P:(DE-2719)2812851$$aRoselli, Francesco$$b8$$udzne
000273977 7001_ $$aBrownstone, Rob$$b9
000273977 7001_ $$aBeato, Marco$$b10
000273977 773__ $$0PERI:(DE-600)2649101-1$$a10.1016/j.celrep.2024.115046$$gVol. 43, no. 12, p. 115046 -$$n12$$p115046$$tCell reports$$v43$$x2211-1247$$y2024
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