| Literature DB >> 29672449 |
Tatsuya Ishikawa1,2, Kei Eto1,3, Sun Kwang Kim1,3,4, Hiroaki Wake1,3,5, Ikuko Takeda1, Hiroshi Horiuchi1, Andrew J Moorhouse6, Hitoshi Ishibashi1,3,7, Junichi Nabekura1,3,8.
Abstract
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.Entities:
Mesh:
Year: 2018 PMID: 29672449 DOI: 10.1097/j.pain.0000000000001248
Source DB: PubMed Journal: Pain ISSN: 0304-3959 Impact factor: 6.961