INCREASE IN SNAP-25 IMMUNOREACTIVITY IN THE MOSSY FIBERS FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA IN THE GERBIL

SNAP-25 (a synaptosomal-associated protein of 25 kDa) has been shown t o be involved both in synaptic vesicle exocytosis and in axonal outgro wth. In the present study, we investigated the changes in SNAP-25 immu noreactivity in the hippocampus of the Mongolian gerbil (Meriones ungu iculatus) at different time points after transient forebrain ischemia insult. In parallel, immunostaining for GAP-43, a protein involved in axonal outgrowth, and for syntaxin-1 (stx1A and stx1B), another protei n implicated in neurotransmitter release, was also analyzed. The anima ls were subjected to 2.5 or 5 min of transient forebrain ischemia thro ugh bilateral common carotid occlusion, and examined at different inte rvals after ischemia. SNAP-25 immunoreactivity was increased in the mo ssy fiber layer as early as 2 days after 5 min of ischemia. Increased SNAP-25 immunoreactivity in mossy fibers was also detected at days 4 a nd 7 after ischemia. On day 15, SNAP-25 staining was similar to that o bserved in control non-ischemic animals. In contrast, no changes in GA P-43 and syntaxin-1 immunoreactivity were observed in the mossy fiber layer following 5 min of ischemia. No modifications in SNAP-25, syntax in-1 or GAP-43 immunoreactivity were observed following 2.5 min of isc hemia, the longest period for which no neuronal damage is observed. Th ese results provide evidence of a specific involvement of SNAP-25 in t he reactive changes associated with transient forebrain ischemia.