Abstract
The physiological role of presynaptic glutamate receptors in controlling presynaptic Ca2+-influx and thereby transmitter release is unknown. To test if presynaptic Ca2+-uptake in the hippocampas is controlled by glutamate autoreceptors, we created a hippocampal slice preparation for investigation of presumed presynaptic Ca2+-signals with ion-sensitive microelectrodes after lesioning of postsynaptic neurons by glucose deprivation. After prolonged glucose deprivation in slices from juvenile animals of postnatal days 13–15 and 20–22, stratum radiatum (SR) and alveus stimulation-induced postsynaptic field potential (fp) components were irreversibly abolished in area CA1, whereas SR stimulation still evoked afferent volleys. Repetitive stimulation of the SR still induced small decreases in the extracellular Ca2+ concentration ([Ca2+]0), but repetitive alveus stimulation no longer induced decreases in [Ca+]0, suggesting a complete damage of pyramidal cells. In lesioned slices the remaining SR stimulation-induced small decreases in [Ca2+]0 presumably reflect presynaptic Ca 2+-influx. These small decreases in [Ca2+]0 were reversibly reduced by kainate, RS-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), N-methyl-d-aspartate (NMDA) and l-glutamic acid (glutamate), without effects on afferent volleys.
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