Kobayashi, S., Yokoyama, S., Maruta, T., Negami, M., Muroyama, A., Mitsumoto, Y., Iwasa, K., Yamada, M. and Yoshikawa, H. (2013) Autoantibody-induced internalization of nicotinic acetylcholine receptor α3 subunit exogenously expressed in human embryonic kidney cells. Journal of Neuroimmunology, 257, 102-106. doi:10.1016/j.jneuroim.2012.12.010

has been cited by the following article:

• TITLE: Attenuation of nicotine-evoked Ca2+ influx by antibody to the nicotinic acetylcholine receptor α3 subunits in human embryonic kidney cells

  AUTHORS: Shota Kobayashi, Shigeru Yokoyama, Takahiro Maruta, Akiko Muroyama, Hiroaki Yoshikawa, Yasuhide Mitsumoto

  KEYWORDS: Nicotinic Acetylcholine Receptor α3 Subunit; Antibody; Endocytosis; Ca2+ Influx; Autoimmune Autonomic Ganglionopathy

  JOURNAL NAME: Advances in Bioscience and Biotechnology, Vol.4 No.6A, June 13, 2013

  ABSTRACT: Autoantibody against neuronal nicotinic acetylcholine receptor (nAChR) α3 subunit is implicated in severe autonomic dysfunction in the patients with autoimmune autonomic ganglionopathy (AAG). Although this autoantibody has been revealed to impair fast excitatory synaptic transmission in autonomic ganglia, its precise mechanism remains unknown. Here, we show that antibody-induced reduction of cell-surface α3 subunits result in impairment of nicotine-evoked Ca2+ influx in stably transfected human embryonic kidney cells. These effects of the antibody were remarkably inhibited by interfering with the endocytic machinery at low-temperature. We conclude that reduction of nAChR in autonomic ganglia can be mediated by the endocytosis of α3 subunits, and resulted in autonomic failure in AAG patients.