Abstract
In the CA1 stratum pyramidale of rat hippocampal slices we have used Ca 2+- and Na +-sensitive microelectrodes to measure the changes in [Ca 2+] o [Na +] o and associated slow field potentials elicited by the iontophoretic application of the excitatory amino acids N- methyl- d-aspartic acid (NMDA), quisqualic acid (Quis), α-amino-3-hydroxy-5-methyl-4-isoazolepropionic acid (AMPA) and glutamic acid (Glu) in the presence of the NMDA receptor antagonists 2-amino-5-phosphonovaleric acid (AP5) and ketamine and the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Although a combination of these antagonists blocked stimulation-induced synaptic field potentials as well as AMPA- and NMDA-induced ionic changes and associated field potentials, Quis-induced ionic changes and associated field potentials could still be observed after 60 min. These residual Quis signals were also resistant to 2-amino-3-phosphonopropionic acid (AP3) and 2-amino-4-phosphonobutyric acid (AP4) suggesting that metabotropic receptors do not play a role in the generation of these signals. We suggest that the receptor class activated under these conditions may play a role in CNQX/AP5-resistant epileptogenesis as well as other pathophysiological conditions.
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