Inter-regional contribution of enhanced activity of the primary somatosensory cortex to the anterior cingulate cortex accelerates chronic pain behavior

Multiple 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 S...

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Bibliographic Details
Published in:The Journal of neuroscience 2011-05, Vol.31 (21), p.7631-7636
Main Authors: Eto, Kei, Wake, Hiroaki, Watanabe, Miho, Ishibashi, Hitoshi, Noda, Mami, Yanagawa, Yuchio, Nabekura, Junichi
Format: Article
Language:English
Subjects:
Action Potentials - physiology
Animals
Brief Communication
Chronic Disease
Gyrus Cinguli - physiology
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neurons - physiology
Pain - physiopathology
Somatosensory Cortex - physiology
Vesicular Inhibitory Amino Acid Transport Proteins - genetics
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Summary:Multiple 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.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.0946-11.2011