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RECORD NUMBER: 361 OF 1241

OLS Field Name OLS Field Data
Main Title Death of Intermediolateral Spinal Cord Neurons Follows Selective, Complement-Mediated Destruction of Peripheral Preganglionic Sympathetic Terminals by Acetylcholinesterase Antibodies.
Author Brimijoin, S. ; Moser, V. ; Hamond, P. ; Oka, N. ; Lennon, V. A. ;
CORP Author ManTech Environmental Technology, Inc., Research Triangle Park, NC. ;Mayo Clinic, Rochester, MN.;National Institutes of Health, Bethesda, MD.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1993
Year Published 1993
Report Number EPA-68-02-4450, NIH-NS-18170;
Stock Number PB93-228914
Additional Subjects Nerve cells ; Spinal cord ; Monoclonal antibodies ; Acetylcholinesterase ; Sympathetic nervous system ; Complement ; Ganglia ; Biochemistry ; Apoptosis ; Electron microscopy ; Reprints ;
Holdings
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Status
NTIS  PB93-228914 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 11/22/1993
Collation 25p
Abstract
Systemically injected anti-acetylcholinesterase antibodies in rats cause selective lesions of preganglionic sympathetic neurons. Adult rats were examined up to four months after a single i.v. injection of murine monoclonal acetylcholinesterase antibodies or normal immunoglobulin G (1.5 mg). Within 4 h, antibody-treated rats developed ptosis, a sign of sympathetic dysfunction that was never reversed. Persistent pupillary constriction reflected preserved and unopposed parasympathetic function. Weight gain was depressed, but locomotor activity, excitability, and sensorimotor responses were normal, and gross neuromuscular performance was near normal. These findings were supported by biochemical evidence for selective sympathetic damage. Acetylcholinesterase activity was reduced for the whole period of observation in sympathetic ganglia and adrenal glands but fell only transiently in muscle and serum. At all times, choline acetyltransferase activity (a marker of presynaptic terminals) was unaffected in muscle but grossly depleted in ganglia. Light and electron microscopy showed that preganglionic sympathetic terminals of superior cervical ganglia were severely damaged while parasympathetic ganglia were less affected and motor endplates of skeletal muscle were apparently spared. Immunocytochemistry revealed punctate deposits of murine immunoglobulin G and complement component C3 in ganglionic neuropil 12 h after antibody injection. (Copyright (c) 1993 IBRO.)