Transient cerebral ischemia induces active astrocytosis without distinct neuronal death in the gerbil main olfactory bulb: a long-term analysis.
In the present study, we examined ischemia-induced neuronal and glial changes in the gerbil MOB at various time points during 60 days after 5 min of transient cerebral ischemia. The number of neuronal neuclei-immunoreactive neurons was not changed after ischemia/reperfusion (I/R). Myelin basic protein immunoreaction was well preserved after I/R. Five days after I/R, reactive form of GFAP-immunoreactive astrocytes began to increase in the external plexiform layer and granule cell layer: These reactive astrocytes peaked 10 days after I/R, thereafter, they decreased with time after I/R. Iba-1-immunoreactive microglia were ubiquitously distributed in all layers of the MOB. After I/R, significant changes in their morphology and immunoreactivity were not detected. The results of western blot analyses for GFAP, Iba-1 and MBP were similar to the immunohistochemical data. In addition, 8-hydroxy-2'-deoxyguanosine (a marker for DNA damage) immunoreactivity and SOD1, an antioxidant, protein levels were not changed in the ischemic MOB. These results indicate that neurons in the MOB are resistant to ischemic insult, showing that astrocytes are activated late in the ischemic MOB.
Choi
Jung Hoon
JH
Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chuncheon, South Korea.
Yoo
Ki-Yeon
KY
Lee
Choong Hyun
CH
Park
Ok kyu
Ok
Yan
Bing Chun
BC
Li
Hua
H
Moon
Yoo Sun
YS
Hwang
In Koo
IK
Lee
Yun Lyul
YL
Shin
Hyung-Cheul
HC
Won
Moo-Ho
MH
D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology*; D016923:Cell Death; D005849:Gerbillinae; D005911:Gliosis; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D002546:Ischemic Attack, Transient / Q000473:pathology*; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D009830:Olfactory Bulb / Q000378:metabolism / Q000473:pathology*