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ttenuates behavioural pain hypersensitivity without the deleteious consequences of directly blocking NMDARs. Thus, understanding of the pathological signalling not only ithin neurons but also in glial cells, and, as well,… Click to show full abstract
ttenuates behavioural pain hypersensitivity without the deleteious consequences of directly blocking NMDARs. Thus, understanding of the pathological signalling not only ithin neurons but also in glial cells, and, as well, the interactions etween neurons and glia within the dorsal horn may lead to novel trategies for the management of chronic pain states, strategies not reviously expected from a solely neuron-centric view of pain. Funding: Supported by the Canadian Institutes of Health esearch, the Krembil Foundation, the Ontario Research Foundaion, and the Howard Hughes Medical Institute.
Journal Title: Scandinavian Journal of Pain
Year Published: 2017
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