Science (New York, N.Y.) · 2010
Alleviating neuropathic pain hypersensitivity by inhibiting PKMzeta in the anterior cingulate cortex.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Li Xiang-Yao, Ko Hyoung-Gon, Chen Tao, Descalzi Giannina, Koga Kohei, Wang Hansen, Kim Susan S, Shang Yuze, Kwak Chuljung, Park Soo-Won, Shim Jaehoon, Lee Kyungmin, Collingridge Graham L, Kaang Bong-Kiun, Zhuo Min
Аннотация
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 (PKMζ) maintains pain-induced persistent changes in the mouse anterior cingulate cortex (ACC). Peripheral nerve injury caused activation of PKMζ in the ACC, and inhibiting PKMζ by a selective inhibitor, ζ-pseudosubstrate inhibitory peptide (ZIP), erased synaptic potentiation. Microinjection of ZIP into the ACC blocked behavioral sensitization. These results suggest that PKMζ in the ACC acts to maintain neuropathic pain. PKMζ could thus be a new therapeutic target for treating chronic pain.
Предметные рубрики MeSH
Adenylyl CyclasesAnalgesicsAnimalsEnzyme InhibitorsExcitatory Postsynaptic PotentialsGyrus CinguliLong-Term PotentiationMaleMemoryMiceMice, Inbred C57BLMice, TransgenicNeuralgiaPatch-Clamp TechniquesPeptidesPeroneal NervePhosphorylationProtein Kinase CReceptors, AMPASensory Receptor CellsSomatosensory CortexSynapsesSynaptic TransmissionProtein Kinase C zeta