期刊
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
卷 146, 期 1-2, 页码 3-7出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.autneu.2008.09.005
关键词
Autonomic neuropathy; Thymoma; Gastrointestinal dysmotility; Orthostatic hypotension
资金
- NINDS NIH HHS [P50 NS032352, P50 NS032352-14, R01NS48077, P50 NS032352-13, P50 NS032352-150004, R01 NS048077-04, R01 NS048077, P50NS32352] Funding Source: Medline
Nicotinic acetylcholine receptors (AChR) are ligand-gated cation channels that are present throughout the nervous system. The ganglionic (alpha 3-type) neuronal AChR mediates fast synaptic transmission in sympathetic, parasympathetic and enteric autonomic ganglia. Autonomic ganglia are an important site of neural integration and regulation of autonomic reflexes. Impaired cholinergic ganglionic synaptic transmission is one important cause of autonomic failure. Ganglionic AChR antibodies are found in many patients with autoimmune autonomic ganglionopathy (AAG). These antibodies recognize the alpha 3 subunit of the ganglionic AChR, and thus do not bind non-specifically to other nicotinic AChR. Patients with high levels of ganglionic AChR antibodies typically present with rapid onset of severe autonomic failure, with orthostatic hypotension, gastrointestinal dysmotility, anhidrosis. bladder dysfunction and sicca symptoms. Impaired pupillary light reflex is often seen. Like myasthenia gravis, AAC is an antibody-mediated neurological disorder. Antibodies from patients with AAG inhibit ganglionic AChR currents and impair transmission in autonomic ganglia. An animal model of AAG in the rabbit recapitulates the important clinical features of the human disease and provides additional evidence that AAG is an antibody-mediated disorder caused by impairment of synaptic transmission in autonomic ganglia. (C) 2008 Elsevier B.V. All rights reserved.
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