期刊
PAIN
卷 159, 期 8, 页码 1592-1606出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/j.pain.0000000000001248
关键词
Astrocyte; Primary somatosensory cortex; Chronic pain; Mirror image pain; Inhibitory neuron; Callosal input; Two-photon microscope
资金
- Core Research for Evolutional Science and Technology (CREST) grant from the Japan Agency for Medical Research and Development (AMED)
- Japan Science and Technology Agency (JST) [22240042, 15K21604, 15K21603, 17K09051, 16H01399, JP16H06280]
- Spectrography and Bioimaging Facility, NIBB Core Research Facilities
Peripheral nerve injury causes maladaptive plasticity in the central nervous system and induces chronic pain. In addition to the injured limb, abnormal pain sensation can appear in the limb contralateral to the injury, called mirror image pain. Because synaptic remodeling in the primary somatosensory cortex (S1) has critical roles in the induction of chronic pain, cortical reorganization in the S1 ipsilateral to the injured limb may also accompany mirror image pain. To elucidate this, we conducted in vivo 2-photon calcium imaging of neuron and astrocyte activity in the ipsilateral S1 after a peripheral nerve injury. We found that cross-callosal inputs enhanced the activity of both S1 astrocytes and inhibitory neurons, whereas activity of excitatory neurons decreased. When local inhibitory circuits were blocked, astrocyte-dependent spine plasticity and allodynia were revealed. Thus, we propose that cortical astrocytes prime the induction of spine plasticity and mirror image pain after peripheral nerve injury. Moreover, this result suggests that cortical synaptic rewiring could be sufficient to cause allodynia on the uninjured periphery.
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