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Cortical astrocytes prime the induction of spine plasticity and mirror image pain

Ishikawa, Tatsuyaa,b; Eto, Keia,c; Kim, Sun Kwanga,c,d; Wake, Hiroakia,c,e; Takeda, Ikukoa; Horiuchi, Hiroshia; Moorhouse, Andrew J.f; Ishibashi, Hitoshia,c,g; Nabekura, Junichia,c,h,*

doi: 10.1097/j.pain.0000000000001248
Research Paper
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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.

When local inhibitory neuronal function was blocked in the S1 ipsilateral to peripheral nerve injury, astrocyte-dependent synaptic remodeling and mirror image pain were induced.

aDivision of Homeostatic Development, National Institute for Physiological Sciences, Okazaki, Japan

bDepartment of Brain Structures and Functions, Faculty of Medical Sciences, University of Fukui, Fukui, Japan

cDepartment of Physiological Sciences, The Graduate School for Advanced Study, Okazaki, Japan

dDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, South Korea

eDivision of System Neuroscience, Kobe University Graduate School of Medicine, Kobe, Japan

fDepartment of Physiology, School of Medical Sciences, The University of New South Wales, Sydney, New South Wales, Australia

gDepartment of Physiology, Kitasato University School of Allied Health Sciences, Sagamihara, Japan

hCore Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama, Japan

Corresponding author. Address: Division of Homeostatic Development, National Institute for Physiological Sciences, Nishigonaka, Myodaiji, Okazaki 444-8585, Japan. Tel.: 81-564-55-7851; fax: 81-564-55-7853. E-mail address: nabekura@nips.ac.jp (J. Nabekura).

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

T. Ishikawa and K. Eto contributed equally to this work.

Received September 25, 2017

Received in revised form April 02, 2018

Accepted April 11, 2018

© 2018 International Association for the Study of Pain
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