Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 7 December 2010
Vol. 3, Issue 151, p. ec372
[DOI: 10.1126/scisignal.3151ec372]


Neuroscience Pain in the Brain

Peter R. Stern

Science, AAAS, Cambridge CB2 1LQ, UK

One of the major challenges in pain research is finding ways to reverse chronic pain. Synaptic long-term potentiation (LTP) at spinal or cortical levels is a cellular model of chronic pain. X.-Y. Li. et al. studied the role of the enzyme protein kinase M zeta (PKM{zeta}) in neurons of the anterior cingulate cortex (ACC) in the maintenance of LTP and for enhanced pain sensitivity after peripheral nerve injury in mice. Nerve injury appeared to lead to the up-regulation and phosphorylation of PKM{zeta}. This triggered LTP at some synapses in the ACC by increasing the number of AMPA receptors. LTP was restricted to ACC neurons that were activated by nerve injury. Blocking PKM{zeta} in the ACC days after nerve injury normalized pain behavior. Thus, PKM{zeta} may represent a promising target for the treatment of chronic pain.

X.-Y. Li, H.-G. Ko, T. Chen, G. Descalzi, K. Koga, H. Wang, S. S. Kim, Y. Shang, C. Kwak, S.-W. Park, J. Shim, K. Lee, G. L. Collingridge, B.-K. Kaang, M. Zhuo, Alleviating neuropathic pain hypersensitivity by inhibiting PKM{zeta} in the anterior cingulate cortex. Science 330, 1400–1404 (2010). [Abstract] [Full Text]

Citation: P. R. Stern, Pain in the Brain. Sci. Signal. 3, ec372 (2010).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882