Effects of neonatal cerebral hypoxia-ischemia on the in vitro phosphorylation of synapsin 1 in rat synaptosomes

Synapsins are phosphoproteins related to the anchorage of synaptic vesicles to the actin skeleton. Hypoxia-ischemra causes an increased calcium influx into neurons through ionic channels gated by activation of glutamate recep tors. In this work seven-day-old Wistar rats were submitted to hypoxia-isch emia and sacrificed after 21 hours, 7, 30, or 90 days. Synaptosomal fractio ns were obtained by Percoll gradients and incubated with P-32 (10 mu Ci/g). Proteins were analysed by SDS-PAGE and radioactivity incorporated into syn apsin 1 was counted by liquid scintillation. Twenty-one hours after hypoxia -ischemia we observed a reduction on the in vitro phosphorylation of synaps in 1, mainly due to hypoxia, rather than to ischemia; this effect was rever sed at day 7 after the insult. There was another decrease in phosphorylatio n 30 days after the event interpreted as a late effect of hypoxia-ischemia. No changes were observed at day 90. Our results suggest that decreased pho sphorylation of synapsin 1 could be related to neuronal death that follows hypoxia-ischemia.