INTRACEREBROVENTRICULAR KAINIC ACID ADMINISTRATION IN ADULT-RAT ALTERS HIPPOCAMPAL CALBINDIN AND NONPHOSPHORYLATED NEUROFILAMENT EXPRESSION

Citation
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
Citations number
70
Categorie Soggetti
Neurosciences
ISSN journal
00219967
Volume
363
Issue
4
Year of publication
1995
Pages
581 - 599
Database
ISI
SICI code
0021-9967(1995)363:4<581:IKAAIA>2.0.ZU;2-P
Abstract
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.