Abstract

The role of IgG in effecting gastrointestinal (G.I.) dysmotility associated with neurologic autoimmunity (idiopathic or paraneoplastic) remains poorly defined. Serum IgG prepared from patients with anti-neuronal nuclear autoantibody type 1 (ANNA-1 [aka anti-Hu], n=7) or ganglionic nicotinic acetylcholine receptor (α3AChR, n=6) autoantibody were tested on myenteric neurons in longitudinal muscle myenteric plexus (LMMP) preparations from the ileum of 38 guinea pigs. IgG prepared from healthy subjects or neurologic patients (n=7) without G.I. symptoms served as controls. Action potential discharges in all neurons of a ganglion in response to acute application of IgG were monitored by fast imaging using a voltage-sensitive dye. Data were analysed as% neurons per ganglion responding and frequency of action potential discharge. Only 0.7±1.2% of 708 neurons (26 ganglia) responded to 2 of 7 control IgG samples (mean action potential frequency 0.5±0.9Hz). Six of 7 samples containing ANNA-1-IgG evoked a response in 7.4±5.7% of 1266 neurons (45 ganglia) (P<0.05) with a significantly higher action potential discharge (1.8±1.1Hz, P<0.05). We observed no correlation between ANNA-1 titer and the percentage of responding neurons or action potential frequency. Four of 6 samples containing α3AChR-IgG evoked a response in a smaller number of neurons (6.5±9.9% of 612 neurons (32 ganglia)) with an action potential frequency of 1.9±1.5Hz.

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