An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia.
Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immunoreactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.
Yoshimi
K
K
New Lead Research Laboratories, Sankyo Co., Ltd., Tokyo, Japan.
Takeda
M
M
Nishimura
T
T
Kudo
T
T
Nakamura
Y
Y
Tada
K
K
Iwata
N
N
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D016923:Cell Death; D002966:Clathrin / Q000378:metabolism*; D005849:Gerbillinae; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism*; D009474:Neurons / Q000473:pathology; D015424:Reperfusion; D013194:Staining and Labeling; D013997:Time Factors
D002966:Clathrin; D008869:Microtubule-Associated Proteins