Neurotransmitter phenotype switching by spinal excitatory interneurons regulates locomotor recovery after spinal cord injury

Author:

Bertels Hannah,Vicente-Ortiz Guillem,El Kanbi Khadija,Takeoka AyaORCID

Abstract

AbstractSevere spinal cord injury in adults leads to irreversible paralysis below the lesion. However, adult rodents that received a complete thoracic lesion just after birth demonstrate proficient hindlimb locomotion without input from the brain. How the spinal cord achieves such striking plasticity remains unknown. In this study, we found that adult spinal cord injury prompts neurotransmitter switching of spatially defined excitatory interneurons to an inhibitory phenotype, promoting inhibition at synapses contacting motor neurons. In contrast, neonatal spinal cord injury maintains the excitatory phenotype of glutamatergic interneurons and causes synaptic sprouting to facilitate excitation. Furthermore, genetic manipulation to mimic the inhibitory phenotype observed in excitatory interneurons after adult spinal cord injury abrogates autonomous locomotor functionality in neonatally injured mice. In comparison, attenuating this inhibitory phenotype improves locomotor capacity after adult injury. Together, these data demonstrate that neurotransmitter phenotype of defined excitatory interneurons steers locomotor recovery after spinal cord injury.

Funder

International Foundation for Research in Paraplegia

Fonds Wetenschappelijk Onderzoek

Wings for Life

GSKE/FMRE Queen Elizabeth Medical Foundation for Neuroscience Young Investigator Grant

Publisher

Springer Science and Business Media LLC

Subject

General Neuroscience

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