神经科学
兴奋性突触后电位
抑制性突触后电位
谷氨酸的
脊髓损伤
脊髓
神经递质
谷氨酸受体
病变
生物
中枢神经系统
医学
病理
受体
生物化学
作者
Hannah Bertels,Guillem Vicente-Ortiz,Khadija El Kanbi,Aya Takeoka
标识
DOI:10.1038/s41593-022-01067-9
摘要
Abstract Severe 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.
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