• Masamichi Shinoda, Satoshi Fujita, Shiori Sugawara, Sayaka Asano, Ryo Koyama, Shintaro Fujiwara, Kumi Soma, Takaaki Tamagawa, Tomoyuki Matsui, Daisuke Ikutame, Masatoshi Ando, Ayaka Osada, Yuki Kimura, Kazutaka Kobayashi, Takamitsu Yamamoto, Kuniko Kusama-Eguchi, Masayuki Kobayashi, Yoshinori Hayashi, and Koichi Iwata.
• Department of Physiology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
• Int J Mol Sci. 2020 Mar 30; 21 (7).

AbstractWe evaluated the mechanisms underlying the spinal cord stimulation (SCS)-induced analgesic effect on neuropathic pain following spared nerve injury (SNI). On day 3 after SNI, SCS was performed for 6 h by using electrodes paraspinally placed on the L4-S1 spinal cord. The effects of SCS and intraperitoneal minocycline administration on plantar mechanical sensitivity, microglial activation, and neuronal excitability in the L4 dorsal horn were assessed on day 3 after SNI. The somatosensory cortical responses to electrical stimulation of the hind paw on day 3 following SNI were examined by using in vivo optical imaging with a voltage-sensitive dye. On day 3 after SNI, plantar mechanical hypersensitivity and enhanced microglial activation were suppressed by minocycline or SCS, and L4 dorsal horn nociceptive neuronal hyperexcitability was suppressed by SCS. In vivo optical imaging also revealed that electrical stimulation of the hind paw-activated areas in the somatosensory cortex was decreased by SCS. The present findings suggest that SCS could suppress plantar SNI-induced neuropathic pain via inhibition of microglial activation in the L4 dorsal horn, which is involved in spinal neuronal hyperexcitability. SCS is likely to be a potential alternative and complementary medicine therapy to alleviate neuropathic pain following nerve injury.

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