• Kei Eto, Hiroaki Wake, Miho Watanabe, Hitoshi Ishibashi, Mami Noda, Yuchio Yanagawa, and Junichi Nabekura.
• Department of Developmental Physiology, Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
• J. Neurosci. 2011 May 25; 31 (21): 7631-6.

AbstractMultiple cortical areas are involved in pain processing, including the primary somatosensory cortex (S1) and the anterior cingulate cortex (ACC). Although accumulations of evidence suggest that the S1 activity increases under chronic pain conditions, whether plastic change occurs or not within the S1, and whether and how the plastic change contributes to chronic pain behavior, is unknown. Here, we provide the first evidence that intra-regional remodeling within the mouse S1 accelerates chronic pain behavior by modulating neuronal activity in the ACC, one of the important cortical areas for chronic pain. Using two-photon Ca(2+) imaging, we found that the spontaneous activity of layer 2/3 neurons in the S1 and then response to sensory and layer 4 stimulations increased under chronic pain conditions. In addition, pharmacological attenuation and facilitation of S1 activity attenuated and facilitated the chronic pain behavior, respectively. Furthermore, electrical response of the ACC to peripheral stimulation successfully correlated with S1 neuronal activity, and inhibition of ACC activity alleviated the mechanical allodynia. The present results will provide development of efficient therapeutic strategies against chronic pain by focusing on the S1 and ACC.

17 keywords...

hide…