Alterations in hippocampal GAP-43, BDNF, and L1 following sustained cerebral ischemia.
Alterations in factors involved in the regeneration of the neuronal network in the hippocampus of rats with microsphere embolism (ME) were examined. Nine hundred microspheres (48 microm in diameter) were injected into the right hemisphere, and immunochemical and immunohistochemical studies on the hippocampus were performed on the seventh day thereafter. Hematoxylin-eosin staining showed progressive and severe degeneration of the hippocampus after ME. The protein levels of brain-derived neurotrophic factor (BDNF), 43-kDa growth-associated protein (GAP-43), and adhesion protein L1 (L1) in the ipsilateral hippocampus of the ME animal, determined by Western blot analysis or enzyme immunoassay, were increased, unaltered, and decreased, respectively. In contrast, the immunohistochemical study showed increases in a marker of axonal sprouting GAP-43, and a neurotrophic factor BDNF, and a decrease in an adhesion molecule L1 in some areas of the hippocampal ischemic penumbra of such animals. These results suggest that some factors for regeneration of the neuronal network in the ischemic penumbra responded to sustained cerebral ischemia for a certain period, although functional network of the nerve cells in the microsphere-injected hemisphere would be unlikely established after ME.
Miyake
Keiko
K
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, 192-0392 Hachioji, Japan.
Yamamoto
Wataru
W
Tadokoro
Mina
M
Takagi
Norio
N
Sasakawa
Kyoko
K
Nitta
Atsumi
A
Furukawa
Shoei
S
Takeo
Satoshi
S
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D002341:Carotid Artery Thrombosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D016923:Cell Death / Q000502:physiology; D002544:Cerebral Infarction / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000502:physiology; D019922:GAP-43 Protein / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D039841:Leukocyte L1 Antigen Complex; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism*; D008863:Microspheres; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009416:Nerve Regeneration / Q000502:physiology*; D019006:Neural Cell Adhesion Molecules / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology
D019208:Brain-Derived Neurotrophic Factor; D019922:GAP-43 Protein; D039841:Leukocyte L1 Antigen Complex; D008562:Membrane Glycoproteins; D019006:Neural Cell Adhesion Molecules