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The in vivo and in vitro influences on glutamate release from hippocampal synapses were investigated by the use of the following experimental procedures: 1) electrotonic interactions between the perforant path (PP) and the cell layers of the hippocampal dentate gyrus (DG); 2) activation of PP inputs to synaptic and nonsynaptic metabotropic and ionotropic receptors; 3) activation of PP inputs to group II metabotropic receptors; and 4) D-2 dopamine receptor antagonism by sulpiride. Activity in the PP caused increases in the apparent release of glutamate from hippocampal synapses in vivo; these increases were blocked by tetrodotoxin and probably were due to activation of neurons in the DG. In vitro, the PP-evoked excitatory postsynaptic potential (EPSP) was blocked by tetrodotoxin and was abolished by intracellular injection of guanine nucleotides, suggesting that the PP-mediated increase in glutamate release was due to the activation of a gamma-aminobutyric acid (GABA)-A/cholinergic receptor. The apparent release of glutamate was increased at PP-DG synapses and lateral PP synapses by stimulation of group II metabotropic receptors. The in vivo increase in glutamate release from PP-DG synapses was blocked by ionotropic NMDA and quisqualate receptors, and by MK-801, but not by tetrodotoxin. A similar block was seen in vitro. The in vivo effects of sulpiride were different from those of MK
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