<P>Synaptic plasticity is a key mechanism for chronic pain. It occurs at different levels of the central nervous system, including spinal cord and cortex. Studies have mainly focused on signaling proteins that trigger these plastic changes, wher...
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https://www.riss.kr/link?id=A107587590
Li, X.-Y. ; Ko, H.-G. ; Chen, T. ; Descalzi, G. ; Koga, K. ; Wang, H. ; Kim, S. S. ; Shang, Y. ; Kwak, C. ; Park, S.-W. ; Shim, J. ; Lee, K. ; Collingridge, G. L. ; Kaang, B.-K. ; Zhuo, M.
2010
-
SCI,SCIE,SCOPUS
학술저널
1400-1404(5쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<P>Synaptic plasticity is a key mechanism for chronic pain. It occurs at different levels of the central nervous system, including spinal cord and cortex. Studies have mainly focused on signaling proteins that trigger these plastic changes, wher...
<P>Synaptic plasticity is a key mechanism for chronic pain. It occurs at different levels of the central nervous system, including spinal cord and cortex. Studies have mainly focused on signaling proteins that trigger these plastic changes, whereas few have addressed the maintenance of plastic changes related to chronic pain. We found that protein kinase M zeta (PKM관) maintains pain-induced persistent changes in the mouse anterior cingulate cortex (ACC). Peripheral nerve injury caused activation of PKM관 in the ACC, and inhibiting PKM관 by a selective inhibitor, 관-pseudosubstrate inhibitory peptide (ZIP), erased synaptic potentiation. Microinjection of ZIP into the ACC blocked behavioral sensitization. These results suggest that PKM관 in the ACC acts to maintain neuropathic pain. PKM관 could thus be a new therapeutic target for treating chronic pain.</P>
Rewiring of Genetic Networks in Response to DNA Damage