Fig. 1.

Paired pre- and postsynaptic activity induces potentiation at the pressure (P)-to-anterior pagoda (AP) synapse. A: schematic of the pairing protocol. Pre- and posttest excitatory postsynaptic potential (EPSP) measurements in the postsynaptic AP cell were obtained by eliciting a single presynaptic (P cell) action potential. Pairing consisted of a 10 pulse train (25 Hz, 10 ms) applied to the P-cell coinciding with a 2 nA step depolarization (500 ms) of the AP cell. Posttest EPSP measurements were completed after a 45 min consolidation period. B: representative EPSP traces prior to (pre) and following pairing (post) from synapses that underwent pairing in normal saline (top) or in MK801 (bottom). The gray trace denotes the pretest EPSP and the black trace denotes the posttest EPSP. C: effects of the N-methyl-d-aspartate receptor (NMDAR) antagonist, MK801, on long-term potentiation (LTP). Pairing-induced LTP was blocked by the application of the NMDAR antagonist MK801 (pairing + MK801). No stimulation and MK801 control groups are significantly different from the pairing group, indicating that potentiation only occurs following coordinated activation of the prepostsynaptic neurons. D: role of glycine during LTP. Elimination of glycine from the bath during the training protocol (pairing, no glycine) or application of 7-chlorokynurenic acid (7-Cl KYNA; pairing +7-Cl KYNA), which blocks the NMDAR glycine binding site, prevented pairing-induced potentiation. Administration of 7-Cl KYNA alone (7-Cl-KYNA control) did not significantly affect baseline synaptic transmission. Asterisks indicates statistically significant difference relative to the pairing group.