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Perturbing PSD-95 Interactions With NR2B-subtype Receptors Attenuates Spinal Nociceptive Plasticity and Neuropathic Pain by D'Mello, Richard; Marchand, Fabien; Pezet, Sophie; McMahon, Stephen B; Dickenson, Anthony H is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Peripheral inflammation or nerve injury induces a primary afferent barrage into the spinal cord, which can cause __N__-methyl -aspartate (NMDA) receptor-dependent alterations in the responses of dorsal horn sensory neurons to subsequent afferent inputs. This plasticity, such as “wind-up” and central sensitization, contributes to the hyperexcitability of dorsal horn neurons and increased pain-related behavior in animal models, as well as clinical signs of chronic pain in humans, hyperalgesia and allodynia. Binding of NMDA receptor subunits by the scaffolding protein postsynaptic density protein-95 (PSD-95) can facilitate downstream intracellular signaling and modulate receptor stability, contributing to synaptic plasticity. Here, we show that spinal delivery of the mimetic peptide Tat-NR2B9c disrupts the interaction between PSD-95 and NR2B subunits in the dorsal horn and selectively reduces NMDA receptor-dependent events including wind-up of spinal sensory neurons, and both persistent formalin-induced neuronal activity and pain-related behaviors, attributed to central sensitization. Furthermore, a single intrathecal injection of Tat-NR2B9c in rats with established nerve injury-induc

Who reads Perturbing PSD-95 Interactions With NR2B-subtype Receptors Attenuates Spinal Nociceptive Plasticity and Neuropathic Pain?

Author

D'Mello, Richard; Marchand, Fabien; Pezet, Sophie; McMahon, Stephen B; Dickenson, Anthony H

Publisher

Nature Publishing Group; Elsevier ; Cell Press; Elsevier BV (ISSN 1525-0016)

Published

2011

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)