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
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.