INTRASYNAPTOSOMAL FREE CALCIUM-CONCENTRATION DURING RAT-BRAIN DEVELOPMENT - EFFECTS OF HYPOXIA, AGLYCAEMIA, AND ISCHEMIA

The effects of hypoxia, aglycaemia, and hypoxia-aglycaemia on intrasyn aptosomal free Ca2+ concentration ([Ca2+](i)) have been investigated i n rat brain synaptosomes prepared from animals aged 5, 10, 15, 20, 25, and 60 days. After 60 min of hypoxia there was no significant differe nce, when compared with controls, in basal [Ca2+](i) or [Ca2+](i) foll owing depolarisation in all of the ages studied. Following 60 min of a glycaemia there was no significant difference from controls in [Ca2+]( i) of synaptosomes prepared from pups of less than or equal to 20 days , although a significant rise in [Ca2+](i) was seen in preparations fr om animals >20 days old. Sixty minutes of hypoxia-aglycaemia led to a significant rise in [Ca2+](i) only in preparations from animals 15-60 days old. With both aglycaemia and hypoxia-aglycaemia a progressive in crease in the magnitude of the rise in [Ca2+](i) was seen with develop ment. These data suggest increases in [Ca2+](i) in adult nerve termina ls following prolonged aglycaemia and hypoxia-aglycaemia but no change following prolonged hypoxia. In contrast, no significant changes in [ Ca2+](i) values were apparent in neonatal nerve terminals under any of these conditions. In control synaptosomes with glucose and oxygen fre ely available, a decrease in resting and depolarised [Ca2+](i) during development was seen, suggesting a change in calcium homeostasis withi n the nerve terminal as the brain develops. It is suggested that the m echanism underlying the relative resistance to ischaemic damage of neo natal brain as compared with adult brain may be related to the regulat ion of calcium at the nerve ending.