Selective destruction of preganglionic sympathetic nerves by antibodies to acetylcholinesterase

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Abstract

Systemic injection of monoclonal antibodies to neural acetyl cholinesterase in rats causes permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensue. In sympathetic ganglia, cholinergic synapses disappear, but postganglionic adrenergic neurones remain structurally and functionally normal. Somatic motor and parasympathetic systems are also spared. This model of selective cholinergic autoimmunity is a new tool for autonomic physiology and may be relevant to the pathogenesis of human dysautonomias.

Original languageEnglish (US)
Pages (from-to)139-145
Number of pages7
JournalJournal of Neural Transmission, Supplement
Issue number34
StatePublished - 1991

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Sympathetic Ganglia
Acetylcholinesterase
Cholinergic Agents
Primary Dysautonomias
Adrenergic Neurons
Adrenal Medulla
Antibodies
Cholinesterases
Syncope
Bradycardia
Autoimmunity
Hypotension
Synapses
Monoclonal Antibodies
Injections

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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abstract = "Systemic injection of monoclonal antibodies to neural acetyl cholinesterase in rats causes permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensue. In sympathetic ganglia, cholinergic synapses disappear, but postganglionic adrenergic neurones remain structurally and functionally normal. Somatic motor and parasympathetic systems are also spared. This model of selective cholinergic autoimmunity is a new tool for autonomic physiology and may be relevant to the pathogenesis of human dysautonomias.",
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AB - Systemic injection of monoclonal antibodies to neural acetyl cholinesterase in rats causes permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensue. In sympathetic ganglia, cholinergic synapses disappear, but postganglionic adrenergic neurones remain structurally and functionally normal. Somatic motor and parasympathetic systems are also spared. This model of selective cholinergic autoimmunity is a new tool for autonomic physiology and may be relevant to the pathogenesis of human dysautonomias.

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