Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability

著者: John M. Dawes, Greg A. Weir, Steven J. Middleton, Ryan Patel, Kim I. Chisholm, Philippa Pettingill, Liam J Peck, J. M. Sheridan, Akila Shakir, Leslie Jacobson, María Gutièrrez‐Mecinas, Jorge Galino, Jan Walcher, Johannes Kühnemund, Hannah Kuehn, Maria Domenica Sanna, Bethan Lang, Alex Clark, Andreas C. Themistocleous, Noboru Iwagaki, Steven J. West, Karolina Werynska, Liam Carroll, Teodora Trendafilova, David A. Menassa, Maria Pia Giannoccaro, Estér Coutinho, Ilaria Cervellini, Damini Tewari, Camilla Buckley, Maria Isabel Leite, Hendrik Wildner, Hanns Ulrich Zeilhofer, Elior Peles, Andrew J. Todd, Stephen B. McMahon, Anthony H. Dickenson, Gary R. Lewin, Angela Vincent, David Bennett - Neuron 2018 被引用: 183

mice. Either immune or genetic-mediated ablation of CASPR2 enhanced the excitability of DRG neurons in a cell-autonomous fashion through regulation of Kv1 channel expression at the soma membrane. This is the first example of passive transfer of an autoimmune peripheral neuropathic pain disorder and demonstrates that CASPR2 has a key role in regulating cell-intrinsic dorsal root ganglion (DRG) neuron excitability.