Fig. 6.

The deficit in 5 Hz LTP in AI rats is not linked to a loss of NMDA receptor function. A, LTP at 5 Hz in young slices [n = 7(4)] is partially NMDA receptor dependent, because bath application of 50 μm APV (hatched bar) depressed but did not completely block LTP triggered by 5 Hz, 30 sec stimulation (Δ).Insets depict the 1st and 150th sweeps recorded from the same slice during the two successive 5 Hz trains. Complex spiking during 5 Hz stimulation in the presence of APV was abolished. After washout, 5 Hz stimulation triggered complex spiking (total spikes, 98 ± 12) and robust LTP that was comparable with that typically seen in naïve control slices (see Fig. 5).B, The NMDA receptor-mediated fEPSP, isolated in the presence of 10 μm CNQX, 10 μm glycine, and 0.2 mm Mg²⁺ was depressed in both AU and AI rats by ∼30% compared with young controls across a range of stimulus intensities [Y, n = 21(7); AU,n = 18(6); AI, n = 13(6)]. When normalized to fiber volley amplitudes >0.5 mV, slope values for both AU and AI rats were significantly different from young controls (p < 0.01). No difference between AU and AI rats was detected. Inset depicts representative traces (average of 5 sweeps) recorded from an aged rat slice before and after exposure to 50 μm APV. Calibration: 1 mV, 10 msec.