EFFECTS OF LOW GLUCOSE-LEVELS ON CHANGES IN [CA2+](O) INDUCED BY STIMULATION OF SCHAFFER COLLATERALS UNDER CONDITIONS OF BLOCKED CHEMICAL SYNAPTIC TRANSMISSION IN RAT HIPPOCAMPAL SLICES

It has been shown previously that hypoxia reduced presumed presynaptic Ca2+ entry in area CA1 of rat hippocampal slices, perhaps due to energy depletion in presynaptic endings. This would imply that hypoglycaemia also affects presynaptic Ca2+ uptake. We therefore studied effects of glucose withdrawal on stimulus induced changes in [Ca2+](0) in area CA1 of rat hippocampal slices. After blockade of synaptic transmission by application of the glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 30 mu M) and L-(+)-2-amino-5-phosphonovaleric acid (2APV, 30 mu M) stimulation of Schaffer collaterals resulted in small but significant reductions in [Ca2+](0) which could be attributed to presynaptic Ca2+ entry. Stimulation of the alveus resulted in somewhat reduced Ca2+ signals mediated to a large extent by Ca2+ entry into dendrites and somatas of pyramidal cells. Removal of glucose results in an augmentation of the presumed presynaptic Ca2+ entry by a factor of 2-3. Decreases in [Ca2+](0) induced by repetitive stimulation of the alveus were initially augmented and then disappeared presumably due to irreversible damage of pyramidal neurones. This finding suggests that depletion of ATP alone does not account for the depressive effect of hypoxia on presynaptic Ca2+ entry.