title: Microsphere embolism-induced elevation of nerve growth factor level and appearance of nerve growth factor immunoreactivity in activated T-lymphocytes in the rat brain.
abstract: Changes in nerve growth factor (NGF) level and type of cells producing NGF were investigated in the rat brain after sustained cerebral embolism. The NGF level was determined by a two-site enzyme immunoassay specific for NGF. The cerebral cortex, striatum, and hippocampus of the embolized hemisphere maximally contained 2.4-, 2.4-, and 1.7-times higher NGF levels than the corresponding regions of the nonembolized hemisphere. A significant increase was transiently observed for 1 week in the cerebral cortex and striatum, whereas the increase was longer lasting, at least of 4 weeks' duration, in the hippocampus. To examine the localization of NGF-like immunoreactivity (NGF-LI), we used a newly developed anti-NGF peptide antiserum that specifically recognized a 30-kDa molecule(s) in the hippocampal extracts or in NGF cDNA-transfected cells, suggesting that the antibody predominantly reacted with the putative NGF precursor protein(s). NGF-LI, which was localized in neurons of the normal or non-embolized hemisphere, was reduced, and on the embolized side new signals emerged in small non-neuronal cells having a round shape. These included cells with common leukocyte antigen CD45 and T-lymphocyte antigen CD3, which did not appear in the normal or non-embolized hemisphere. NGF-LI and CD3 were colocalized in a substantial number of the cells, suggesting that some activated T-lymphocytes produce NGF for neuronal regeneration after sustained cerebral embolism.
authors.affiliation: Department of Pharmacology, Tokyo University of Pharmacy & Life Science, Hachioji, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Mizuma
authors.forename: K
authors.initials: K
authors.lastname: Takagi
authors.forename: K
authors.initials: K
authors.lastname: Miyake
authors.forename: N
authors.initials: N
authors.lastname: Takagi
authors.forename: K
authors.initials: K
authors.lastname: Ishida
authors.forename: S
authors.initials: S
authors.lastname: Takeo
authors.forename: A
authors.initials: A
authors.lastname: Nitta
authors.forename: H
authors.initials: H
authors.lastname: Nomoto
authors.forename: Y
authors.initials: Y
authors.lastname: Furukawa
authors.forename: S
authors.initials: S
authors.lastname: Furukawa
mesh_terms: D000818:Animals; D001921:Brain / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D003342:Corpus Striatum / Q000378:metabolism; D007839:Functional Laterality; D006624:Hippocampus / Q000378:metabolism; D007124:Immunoenzyme Techniques; D002542:Intracranial Embolism and Thrombosis / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D017493:Leukocyte Common Antigens / Q000032:analysis; D008213:Lymphocyte Activation; D008297:Male; D008863:Microspheres; D009414:Nerve Growth Factors / Q000032:analysis / Q000378:metabolism*; D020933:Neurotrophin 3; D051381:Rats; D017208:Rats, Wistar; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D013997:Time Factors
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D009414:Nerve Growth Factors; D020933:Neurotrophin 3; D017493:Leukocyte Common Antigens