Editors' ChoiceNeuroscience

Pain in the Brain

See allHide authors and affiliations

Science Signaling  07 Dec 2010:
Vol. 3, Issue 151, pp. ec372
DOI: 10.1126/scisignal.3151ec372

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 (PKMζ) 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 PKMζ. 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 PKMζ in the ACC days after nerve injury normalized pain behavior. Thus, PKMζ 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 PKMζ in the anterior cingulate cortex. Science 330, 1400–1404 (2010). [Abstract] [Full Text]

Stay Connected to Science Signaling