BIPHASIC CHANGES IN F3 CONTACTIN EXPRESSION IN THE GERBIL HIPPOCAMPUSAFTER TRANSIENT ISCHEMIA/

Citation
H. Cho et al., BIPHASIC CHANGES IN F3 CONTACTIN EXPRESSION IN THE GERBIL HIPPOCAMPUSAFTER TRANSIENT ISCHEMIA/, Experimental Brain Research, 122(2), 1998, pp. 227-234
Citations number
35
Categorie Soggetti
Neurosciences
ISSN journal
00144819
Volume
122
Issue
2
Year of publication
1998
Pages
227 - 234
Database
ISI
SICI code
0014-4819(1998)122:2<227:BCIFCE>2.0.ZU;2-Q
Abstract
We studied changes in expression of F3/contactin (F3), a neuron-specif ic adhesion molecule, in the gerbil hippocampus after transient forebr ain ischemia for 5 min. By immunohistochemical techniques using F3 ant ibody, we found a biphasic change in immunoreactivity for F3 in the CA I area after ischemia. Western blotting of F3 protein showed a similar biphasic change. F3 immunoblots decreased to 67% of the control at 1 week, but then they increased and attained 159% at 3 weeks and 152% at 5 weeks after ischemia. Immunoreactivity of a neurofilament (NF145) s howed a similar biphasic change to F3 but to a lesser extent. In contr ast, microtubule-associated protein 2 (MAP2) immunoreactivity uniforml y decreased after ischemia. In situ hybridization revealed that F3 mes senger RNA (mRNA) hybridization signals in CA1 area were greatly reduc ed 1 week after ischemia, while the signals in the CA3 area were uncha nged and even increased 3 weeks after ischemia. Damage to CA3 neurons by hyperthermic ischemia blocked the F3 increase in area CAI. Our resu lts suggest that the initial decrease in F3 following ischemia reflect s loss of CA1 neurons and the late increase in F3, which shows that a similar time course with neurofilaments may be caused by neurite sprou ting.