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-ischemia causes an increased calcium influx into neurons through ionic channels gated by activation of glutamate receptors. In this work seven-day-old Wistar rats were submitted to hypoxia-ischemia and sacrificed after 21 hours, 7, 30, or 90 days. Synaptosomal fractions were obtained by Percoll gradients and incubated with 32P (10 microCi/g). Proteins were analysed by SDS-PAGE and radioactivity incorporated into synapsin 1 was counted by liquid scintillation. Twenty-one hours after hypoxia-ischemia we observed a reduction on the in vitro phosphorylation of synapsin 1, mainly due to hypoxia, rather than to ischemia; this effect was reversed at day 7 after the insult. There was another decrease in phosphorylation 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 phosphorylation of synapsin 1 could be related to neuronal death that follows hypoxia-ischemia.
Moretto
M B
MB
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
de Mattos-Dutra
A
A
Arteni
N
N
Meirelles
R
R
de Freitas
M S
MS
Netto
C A
CA
Pessoa-Pureur
R
R
D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D016923:Cell Death; D005260:Female; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000473:pathology; D008297:Male; D010766:Phosphorylation; D051381:Rats; D017208:Rats, Wistar; D016704:Synapsins / Q000378:metabolism*; D013574:Synaptosomes / Q000378:metabolism*
D016704:Synapsins