DEVELOPMENTAL AND PLASTICITY-RELATED DIFFERENTIAL EXPRESSION OF 2 SNAP-25 ISOFORMS IN THE RAT-BRAIN

Citation
U. Boschert et al., DEVELOPMENTAL AND PLASTICITY-RELATED DIFFERENTIAL EXPRESSION OF 2 SNAP-25 ISOFORMS IN THE RAT-BRAIN, Journal of comparative neurology, 367(2), 1996, pp. 177-193
Citations number
50
Categorie Soggetti
Neurosciences
ISSN journal
00219967
Volume
367
Issue
2
Year of publication
1996
Pages
177 - 193
Database
ISI
SICI code
0021-9967(1996)367:2<177:DAPDEO>2.0.ZU;2-X
Abstract
In this article we study the relationship between the expression patte rn of two recently identified isoforms of the 25-kD synaptosamal-assoc iated protein (SNAP-25a and SNAP-25b) and the morphological changes in herent to neuronal plasticity during development and kainic acid treat ment. SNAP-25 has been involved in vescicle fusion in the nerve termin al, and most likely participates in different membrane fusion-related processes, such as those involved in neurotransmitter release and axon al growth. In the adult brain, SNAP-25b expression exceeded SNAP-25a i n distribution and intensity, being present in most brain structures. Moderate or high levels of SNAP-25a hybridization signal were found in neurons of the olfactory bulb, the layer Va of the frontal and pariet al cortices, the piriform cortex, the subiculum and the hippocampal CA 4 field, the substantia nigra/pars compacta, and the pineal gland, par tially overlapping SNAP-25b mRNA distribution. In restricted regions o f cerebral cortex, thalamus, mammillary bodies, substantia nigra, and pineal glands the two isoforms were distributed in reciprocal fashion. During development SNAP-25a mRNA was the predominant isoform, whereas SNAP-25b expression increased postnatally. The early expression of SN AP-25a in the embryo and the decrease after P21 is suggestive of a pot ential involvement of this isoform in axonal growth and/or synaptogene sis. This conclusion is indirectly supported by the observation that S NAP-25a mRNA, but not SNAP-25b mRNA, was upregulated in the granule ce lls of the adult dentate gyrus 48 hours after kainate-induced neurotox ic damage of the hippocampal CA3-CA4 regions. Increase of SNAP-25 immu noreactivity was observed as early as 4 days after kainate injection w ithin the messy fiber terminals of the CA3 region, and in the newly fo rmed messy fiber aberrant terminals of the supragranular layer. These data suggest an isoform-specific role of SNAP-25 in neural plasticity. (C) 1996 Wiley-Liss, Inc.