Figure 2.

Estradiol selectively facilitates AMPA receptor-mediated components of fast EPSPs. A, Pharmacologically isolated IPSPs (responses recorded in the presence of 20 μm DNQX and 100 μm APV, antagonists for AMPA and NMDA receptors, respectively) were elicited by stimulation of the Schaffer–commissural projections. These responses were completely blocked by the GABA_A receptor antagonist picrotoxin (PTX, upper right traces) and were unaffected by infusions of 1 nm E2 (upper left traces; also see text). Paired-pulse depression (200 ms interstimulus interval), a characteristic feature of fast IPSPs (see text), was unaffected by E2 (upper left traces and graph); subsequent infusion of the presynaptic GABA_B receptor antagonist saclofen (100 μm) (upper right traces and graph) confirmed that the depression was due to GABA autoreceptors (n = 5). Calibration: 0.1 mV, 50 ms. B, The NMDA receptor component of the fEPSP was isolated by incubating the slices with 20 μm DNQX and 100 μm PTX. The resultant evoked potentials were unaffected by 20 min infusions of 1 nm E2 and were eliminated by APV (n = 4). The traces included in the inset illustrate the slow kinetics of the isolated NMDA response (calibration: 0.1 mV, 20 ms) and the extent to which it is insensitive to E2. C, E2 (1 nm) enhances isolated AMPA-receptor-mediated fEPSPs. The graph summarizes the results for a group of slices (n = 4) tested in the presence of APV and PTX. E2 (1 nm) caused an ∼20% increase in the amplitude of the isolated AMPA receptor-mediated fEPSP, a value comparable to that obtained in untreated slices (see Fig. 1). The traces included in the inset illustrate the E2 effect and the extent to which the responses were eliminated by the AMPA receptor antagonist DNQX.