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Immunoglobulin Fcγ receptor promotes immunoglobulin uptake, immunoglobulin‐mediated calcium increase, and neurotransmitter release in motor neurons
Author(s) -
Mohamed Habib A.,
Mosier Dennis R.,
Zou Ling L.,
Siklós László,
Alexianu Maria E.,
Engelhardt Jozsef I.,
Beers David R.,
Le Weidong,
Appel Stanley H.
Publication year - 2002
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10271
Subject(s) - immunoglobulin g , axon , neurotransmitter , acetylcholine receptor , motor neuron , calcium in biology , neuromuscular junction , intracellular , antibody , immunoglobulin superfamily , microbiology and biotechnology , chemistry , motor nerve , biology , acetylcholine , neuroscience , receptor , immunology , endocrinology , biochemistry , spinal cord
Receptors for the Fc portion of immunoglobulin G (IgG; FcγRs) facilitate IgG uptake by effector cells as well as cellular responses initiated by IgG binding. In earlier studies, we demonstrated that amyotrophic lateral sclerosis (ALS) patient IgG can be taken up by motor neuron terminals and transported retrogradely to the cell body and can alter the function of neuromuscular synapses, such as increasing intracellular calcium and spontaneous transmitter release from motor axon terminals after passive transfer. In the present study, we examined whether FcγR‐mediated processes can contribute to these effects of ALS patient immunoglobulins. F(ab′) 2 fragments (which lack the Fc portion) of ALS patient IgG were not taken up by motor axon terminals and were not retrogradely transported. Furthermore, in a genetically modified mouse lacking the γ subunit of the FcR, the uptake of whole ALS IgG and its ability to enhance intracellular calcium and acetylcholine release were markedly attenuated. These data suggest that FcγRs appear to participate in IgG uptake into motor neurons as well as IgG‐mediated increases in intracellular calcium and acetylcholine release from motor axon terminals. © 2002 Wiley‐Liss, Inc.