We examined the distribution of
synapsin I in the gerbil brain and investigated ischemic damage of presynaptic terminals immunohistochemically by using this
protein as a marker
protein of synaptic vesicles. The reaction for
synapsin I in normal gerbil brain is exclusively localized in the neuropil, and other brain structures such as neuronal
soma, dendrites, axon bundles, glia and endothelial cells exhibited little immunoreactivity. In a reproducible gerbil model of unilateral
cerebral ischemia, ischemic loss of
synapsin I immunoreactivity in the affected hemisphere was confined to the area exhibiting overt
infarction, where the breakdown of this
protein was also confirmed by the immunoblot analysis, and noted much later than that of
microtubule-associated protein 2 immunoreactivity, which was demonstrated in neuronal
soma and dendrites. In the non-affected hemisphere, selective damage of presynaptic terminals due to
Wallerian degeneration and subsequently occurring resynaptogenesis at the molecular layer of the dentate gyrus were clearly demonstrated as a loss and recovery of immunoreaction for
synapsin I, respectively. In a gerbil model of bilateral
cerebral ischemia, immunoreaction for
synapsin I was persistently preserved after seven days to two months recirculation following a brief period of global forebrain
ischemia in the CA1 region of the hippocampus, where delayed neuronal death was consistently observed.(ABSTRACT TRUNCATED AT 250 WORDS)