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Maladaptive Synaptogenesis induced by interaction of voltage gated calcium channel subunit alpha2delta-1 and thrombospondin-4 represents a new mechanism underlying neuropathic pain processing in nerve injury models

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The molecular basis of neuropathic pain is poorly understood. We have previously shown that nerve injury induces increased production of thrombospondin-4 and voltage-gated calcium channel subunit α2δ-1 and that these proteins play a critical role in mediating behavioral hypersensitivity in animal models. However, the mechanism of action has not been elucidated. I use immunohistochemical staining in nerve injured animal model spinal cords to show that interaction of thrombospondin-4 with α2δ-1 promote excitatory synaptogenesis. Furthermore, I use immunocytochemistry staining in spinal cord and dorsal root ganglia neuron co-culture to show that thrombospondins-4/α2δ-1 interaction mediated synaptogenesis depends on pre-synaptic T-type voltage-gated calcium channel function.

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