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Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Ca v α 2 δ 1 subunits and involving T‐type Ca 2+ channels
Author(s) -
Yu Yanhui Peter,
Gong Nian,
Kweon Tae Dong,
Vo Benjamin,
Luo Z David
Publication year - 2018
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.14149
Subject(s) - synaptogenesis , postsynaptic potential , neuroscience , gabapentin , spinal cord , neuropathic pain , excitatory postsynaptic potential , excitatory synapse , chemistry , microbiology and biotechnology , biology , medicine , inhibitory postsynaptic potential , pathology , receptor , biochemistry , alternative medicine
Nerve injury induces concurrent up-regulation of the voltage-gated calcium channel subunit Ca v α 2 δ 1 and the extracellular matrix protein thrombospondin-4 (TSP4) in dorsal root ganglia and dorsal spinal cord, leading to the development of a neuropathic pain state. Interactions of these proteins promote aberrant excitatory synaptogenesis that contributes to neuropathic pain state development through unknown mechanisms. We investigated the contributions of Ca v α 2 δ 1 subunits and TSP4 to synaptogenesis, and the pathways involved in vitro, and whether treatment with gabapentin could block this process and pain development in vivo.