Journal
EXPERIMENTAL NEUROLOGY
Volume 358, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2022.114220
Keywords
Perineuronal nets; Link protein 1; Plasticity; Locomotion; Spinal cord injury
Categories
Funding
- Fundacio La Marato-TV3 [TV3-20173630-31]
- European Union (ERDF/ESF, Investing in your future)
- AGAUR, Secretaria d'Universitats i Recerca del Departament d'Empresa i Coneixement de la Generalitat de Catalunya
- PIF UAB fellowship
- Ministerio de Economia y Competitividad y Fondo Europeo de Desarrollo Regional [RTI2018-101105B-I00]
- European Social Funds
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This study aims to elucidate the role of spinal PNNs on motor function and plasticity. Lack of Crtl1 can lead to disorganized PNNs, altering excitatory synapses and affecting the physiological properties of motoneurons, resulting in motor impairments.
Perineuronal nets (PNNs) are a specialized extracellular matrix that have been extensively studied in the brain. Cortical PNNs are implicated in synaptic stabilization, plasticity inhibition, neuroprotection, and ionic buffering. However, the role of spinal PNNs, mainly found around motoneurons, is still unclear. Thus, the goal of this study is to elucidate the role of spinal PNNs on motor function and plasticity in both intact and spinal cord injured mice. We used transgenic mice lacking the cartilage link protein 1 (Crtl1 KO mice), which is implicated in PNN assembly. Crtl1 KO mice showed disorganized PNNs with an altered proportion of their components in both motor cortex and spinal cord. Behavioral and electrophysiological tests revealed motor impairments and hyperexcitability of spinal reflexes in Crtl1 KO compared to WT mice. These functional outcomes were accompanied by an increase in excitatory synapses around spinal motoneurons. Moreover, following spinal lesions of the corticospinal tract, Crtl1 KO mice showed increased contralateral sprouting compared to WT mice. Altogether, the lack of Crtl1 generates aberrant PNNs that alter excitatory synapses and change the physiological properties of motoneurons, overall altering spinal circuits and producing motor impairment. This disorganization generates a permissive scenario for contralateral axons to sprout after injury.
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