Document Detail


Recovery of cholinergic phenotype in the injured rat neostriatum: roles for endogenous and exogenous nerve growth factor.
MedLine Citation:
PMID:  1431899     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Polyclonal antibodies against recombinant human nerve growth factor (rhNGF) potently inhibited PC12 neurite outgrowth, blocked high-affinity 125I-rhNGF binding but not its receptor, and cross-reacted with rat, mouse, and human nerve growth factor (NGF) but not with brain-derived neurotrophic factor, neurotrophin-3, ciliary neurotrophic factor, insulin-like growth factor, epidermal growth factor, or activin A. Immunocytochemistry revealed many NGF-positive neurons in the rat neostriatum. The NGF-positive neurons disappeared by 3 days after mechanical injury to the neostriatum and were replaced by intensely NGF- and glial fibrillary acidic protein-positive astrocytes. Enzyme-linked immunosorbent assay measurements revealed that the NGF content of the injured striatum was elevated by eightfold 3 days postinjury and by twofold 2 weeks later. The high-affinity choline uptake (HACU) into cholinergic nerve terminals was decreased by 23% at 2 and 4 weeks postinjury, yet choline acetyltransferase (ChAT) activity in these neurons was unchanged at 2 weeks and decreased by 14% at 4 weeks. Daily infusion of 1 microgram of rhNGF into the injury area did not alter the loss of HACU. However, this treatment elevated ChAT activity by 23-29% above intact neostriatal levels and by 53-65% relative to HACU at both survival times. Thus, lesion-induced increases in NGF levels within astrocytes are associated with maintenance of striatal ChAT activity at normal levels following cholinergic injury, even with decreases in HACU. Pharmacologic doses of rhNGF can further augment ChAT activity in damaged cholinergic neurons, showing the usefulness of exogenous NGF even when endogenous NGF is elevated in response to injury.
Authors:
C A Altar; M Armanini; M Dugich-Djordjevic; G L Bennett; R Williams; S Feinglass; V Anicetti; D Sinicropi; C Bakhit
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  59     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  1992 Dec 
Date Detail:
Created Date:  1992-12-22     Completed Date:  1992-12-22     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2167-77     Citation Subset:  IM    
Affiliation:
Developmental Biology, Genentech, Inc., South San Francisco, California.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies / analysis,  immunology
Antibody Specificity
Astrocytes / chemistry,  enzymology
Choline / metabolism
Choline O-Acetyltransferase / metabolism*,  physiology
Dose-Response Relationship, Drug
Enzyme-Linked Immunosorbent Assay
Glial Fibrillary Acidic Protein / analysis
Humans
Immunohistochemistry
Iodine Radioisotopes
Male
Neostriatum / chemistry,  enzymology*,  injuries*
Nerve Growth Factors / immunology,  pharmacology*,  physiology*
Neurons / chemistry,  enzymology
PC12 Cells
Phenotype
Rats
Rats, Inbred F344
Recombinant Proteins / immunology,  pharmacology
Stress, Mechanical
Chemical
Reg. No./Substance:
0/Antibodies; 0/Glial Fibrillary Acidic Protein; 0/Iodine Radioisotopes; 0/Nerve Growth Factors; 0/Recombinant Proteins; 62-49-7/Choline; EC 2.3.1.6/Choline O-Acetyltransferase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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