TAFA4 relieves injury-induced mechanical hypersensitivity through LDL receptors and modulation of spinal A-type K+ current
Sungjae Yoo, Catarina Santos, Ana Reynders, Irène Marics, Pascale Malapert, Stéphane Gaillard, Aude Charron, Sophie Ugolini, Rafaëlle Rossignol, Abderazzak El Khallouqi, Jean–Yves Springael, Marc Parmentier, Andrew J. Saurin, Jean‐Marc Goaillard, Francis Castets, Nadine Clerc, Aziz Moqrich
Abstract
) in lamina II inner inhibitory interneurons (L-IIi InhINs). Remarkably, SNI-induced ion current alterations in both IN subtypes were rescued by TAFA4 in an LRP-dependent manner. We provide insights into the mechanism by which TAFA4 reverses injury-induced mechanical hypersensitivity by restoring normal spinal neuron activity and highlight the considerable potential of TAFA4 as a treatment for injury-induced mechanical pain.
Topics & Concepts
SNiNerve injuryExcitatory postsynaptic potentialReceptorInhibitory postsynaptic potentialNeuropathic painMedicineAnalgesicNeuroscienceHyperalgesiaPharmacologyChemistryInternal medicineBiologyNociceptionAnesthesiaBiochemistryHydrolysisAcid hydrolysisPain Mechanisms and TreatmentsIon channel regulation and functionNeuroscience and Neuropharmacology Research