ALTERATIONS OF AMPA-SELECTED GLUTAMATE SUBTYPE IMMUNOREACTIVITY IN THE DENTATE GYRUS AFTER PERFORANT PATHWAY LESION

Citation
K. Mizukami et al., ALTERATIONS OF AMPA-SELECTED GLUTAMATE SUBTYPE IMMUNOREACTIVITY IN THE DENTATE GYRUS AFTER PERFORANT PATHWAY LESION, Brain research, 768(1-2), 1997, pp. 354-360
Citations number
17
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
768
Issue
1-2
Year of publication
1997
Pages
354 - 360
Database
ISI
SICI code
0006-8993(1997)768:1-2<354:AOAGSI>2.0.ZU;2-I
Abstract
Immunocytochemical techniques were employed to examine the changes in immunolabeling of the lpha-amino-3-hydroxy-5-methyl-4-isoaxolepropiona te (AMPA) receptor subunits GluR1 and GluR2/3 within the dentate gyrus 1, 3, 7, 14, 30, and 90 days after a unilateral perforant pathway les ion in the rat brain. Completeness of the lesion was confirmed followi ng examination of Nissl-stained tissue sections at all times post-lesi on and acetylcholinesterase (AChE)-stained sections 14, 30 and 90 days post-lesion, the latter providing evidence of compensatory sprouting of cholinergic fibers in the outer molecular layer of the dentate gyru s. Compared to the non-lesioned hippocampus there was no difference in the staining pattern of AMPA receptor subunits in the dentate gyrus o f the deafferented hippocampus 1, 3, 7 and 14 days following lesioning of the perforant pathway. In contrast, 30 and 90 days post-lesion, Gl uR1 immunolabeling was increased in the outer molecular layer of the d entate gyrus (i.e., deafferented zone) ipsilateral to lesion. Likewise , GluR2/3 immunolabeling was increased within the same region although the intensity of the response was less than that which was observed f or GluR1. These data suggest that the loss of the perforant pathway fi bers results in a compensatory increase in GluR1 and to a lesser exten t GluR2/3 immunolabeling of the outer molecular layer at 30 and 90 day s post-lesion and further suggest that AMPA receptor subunits play a r ole in perforant pathway signal transduction. (C) 1997 Elsevier Scienc e B.V.