Glutamate secretion and NAD(P)H levels during calcium-dependent depolarization of slices of the dentate gyrus.
Evidence from studies involving release, postsynaptic responses, inactivation, storage and synthesis etc. support the contention that glutamate may be the transmitter of the perforant input to the granule cells in the dentate gyrus of the hippocampus. In the present report the release of endogenous glutamate and the levels of reduced pyridine nucleotides (NAD(P)H) has been measured in parallel experiments on slices from the dentate gyrus of the hippocampus. A Ca-dependent release of glutamate is evoked by tissue depolarization caused either with electrical field stimulation or with elevated KC1. Electrical stimulation induced a transient increase in tissue NAD(P)H levels, the increase being inhibited by approximately 50% during Ca-free conditions. KC1 stimulation, on the other hand, produced a long-lasting decrease in NAD(P)H, the decrease being halved in the absense of Ca. A metabolic relation between stimulus secretion and energy utilization is discussed.
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D046508:Culture Techniques; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D005971:Glutamates / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism*; D009249:NADP / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D009435:Synaptic Transmission / Q000187:drug effects*
D005971:Glutamates; D009249:NADP; D011188:Potassium; D002118:Calcium