Ak. Shetty et Da. Turner, INTRACEREBROVENTRICULAR KAINIC ACID ADMINISTRATION IN ADULT-RAT ALTERS HIPPOCAMPAL CALBINDIN AND NONPHOSPHORYLATED NEUROFILAMENT EXPRESSION, Journal of comparative neurology, 363(4), 1995, pp. 581-599
Calbindin and non-phosphorylated neurofilament proteins were assessed
in hippocampus following a unilateral intracerebroventricular kainic a
cid injection at 4, 26, and 60 days post-lesion, using immunocytochemi
cal expression. The density of calbindin-positive nonpyramidal neurons
throughout the hippocampus showed no significant alteration at 4 days
post-lesion, a significant decrease at 26 days post-lesion, and a par
tial recovery at 60 days post-lesion. In addition, calbindin immunorea
ctivity was dramatically reduced at 26 days post-lesion in the CA1 pyr
amidal and dentate granule cell layers and the messy fibers, bilateral
ly. Although not significant statistically, most of these reductions s
howed signs of reversal at 60 days post-lesion except the CA1 pyramida
l cell layer where the dramatic reductions persisted. Neurofilaments w
ere also altered throughout the post-lesion period, particularly in ab
normal expression of non-phosphorylated neurofilament proteins in mess
y fibers. The apparent return of calbindin immunoreactivity in non-pyr
amidal neurons by 60 days post-lesion suggests that recovery from the
lesion may involve remaining neuronal elements which either become rea
ctivated with time or have the capability to express normal levels of
calbindin with re-innervation. On the other hand, prolonged calbindin
reductions in superficial CA1 pyramidal cells suggest sustained down-r
egulation of calbindin expression owing to persistent reductions in th
e activity of these neurons. The temporal correlation of the expressio
n of non-phosphorylated neurofilaments in messy fibers with their spro
uting response following target loss suggests a potential role for non
-phosphorylated neurofilaments in neuronal plasticity involving axonal
sprouting. Alternatively, it may also suggest that injury-induced neu
rofilament modifications are either conducive or permissive for axonal
sprouting. (C) 1995 Wiley-Liss, Inc.