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. Author manuscript; available in PMC: 2011 Dec 22.
Published in final edited form as: Neuron. 2010 Dec 22;68(6):1143–1158. doi: 10.1016/j.neuron.2010.11.034

Figure 1. AMPAR blockade induces a state-dependent enhancement of presynaptic function.

Figure 1

(A–C) Representative recordings (A) and mean (+ SEM) mEPSC amplitude (B) and frequency (C) of experiments (27–40 DIV) from the following conditions (24 hr): Control (n = 13), 10 μM NBQX (n = 9), 2 μM TTX (n = 10), TTX+NBQX (n = 8). 24 hr NBQX increases both mEPSC amplitude and frequency (*p < 0.05, relative to control); AP blockade prevents the increase in mEPSC frequency induced by AMPAR blockade, but not changes in mEPSC amplitude. (D–F) Representative recordings (D) and mean (+ SEM) mEPSC amplitude (E) and frequency (F) of experiments (21–38 DIV) from the following conditions (3 hr): Control (n = 10), 40 μM CNQX (n = 12), 2 μM TTX (n = 10), and TTX+CNQX (n = 11). Brief AMPAR blockade induces a significant (*p < 0.05, relative to control) increase in both mEPSC amplitude and frequency; AP blockade prevents the increase in mEPSC frequency induced by AMPAR blockade, but not changes in mEPSC amplitude. (G) Representative examples and (H) mean (+SEM) normalized surface GluA1 expression at excitatory synapses (21–40 DIV) from the following conditions (3 hr): Controls (n = 46), CNQX (n = 44), TTX (n = 48), or CNQX+TTX (n = 46). Brief AMPAR blockade significantly (*p < 0.05, relative to control) enhances postsynaptic surface GluA1 expression in the presence or absence of background spiking. (I–J) Representative examples and mean (+SEM) proportion of vglut1-positive excitatory presynaptic terminals with corresponding syt-lum signal from the indicated treatment groups (DIV 37–40). Left to right n = 54, 49, 52, 50, 64, 68, 64, 67 images. Brief AMPAR blockade significantly (*p < 0.05, relative to control) enhances synaptic syt-lum uptake which is prevented by coincident AP (+TTX) or P/Q/N-Ca2+ channel (+CTx/ATx) blockade. (K) Example traces and (L) mean (± SEM) paired-pulse facilitation (PPF), defined as the percent increase in peak amplitude of EPSC2 relative to EPSC1 at different inter-pulse intervals. AMPAR blockade (CNQX alone; n = 29 neurons) produced a significant (*p < 0.05, relative to control; n = 29 neurons) decrease in PPF; co-application of TTX during AMPAR blockade (n = 29 neurons) restored PPF to control levels. The dashed line represents peak amplitude of EPSC1. Scale bars = 25 pA, 50 ms.