Abstract

The effects of glucose deprivation were studied in area CA1 of rat hippocampal slices obtained from adult and juvenile rats (postnatal days (PN) 6–8; 13–15; 20–22). Ion-sensitive microelectrodes were employed to monitor baseline and stimulus-induced changes in [Ca 2+] 0, [K +] 0 and field potentials. In slices from juvenile animals, the decline of baseline [Ca 2+] 0 during glucose deprivation was delayed in comparison to adult slices. The minimum in [Ca 2+] 0 was reached in slices from adult rats after 50±8.5 min, in slices from PN 20–22 after 69±9 min, and in slices from PN 13–15 after 111±11 min. In slices from PN 6–8, [Ca 2+] 0 did not decrease significantly even during prolonged exposure of up to 4 h. Alvear stimulation failed to evoke any stimulus-induced responses in field potentials, rises in [K +] 0 and decreases in [Ca 2+] 0 after the minimum in [Ca 2+] 0 was reached in slices from all age groups except for slices from PN 6–8. In the older age groups, afferent fibre stimulation still induced afferent volleys and small decreases in [Ca 2+] 0, which were about 20–30% of those under control conditions, suggesting that presynaptic fibres and endings maintained some of their functional properties even after prolonged glucose deprivation. In contrast, stimulation of the stratum radiatum failed to evoke synaptic responses in slices from PN 6–8, presumably due to a failure in synaptic transmission. These findings confirm that similar to hypoxia during the early postnatal stage, hippocampal neurons are much more resistant to glucose deprivation. The findings also show that during early postnatal development, glucose deprivation may result in a block of synaptic transmission independent of postsynaptic excitability.

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