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. 2008 Jan 3;105(2):746–750. doi: 10.1073/pnas.0709407105

Fig. 3.

Fig. 3.

Internal application of blockers of either vacuolar H+-ATPase or SNARE-dependent vesicular fusion suppresses DISC. Either bafilomycin A1 (500 nM) (a) or BoTxD (100 nM) (b) was added to the internal saline. [Calibration bar: 300 pA, 2 sec (current trace).] The high-pass-filtered traces are displayed by using a range of −25 to 25 pA (a Lower). For control experiments to address side effects on mGluR1/TrpC1 signaling, an mGluR1 agonist, DHPG (150 μM), together with glutamate (10 μM), was pressure-ejected (10 psi, 50 msec) in the inner one-third of the molecular layer to induce both fast (AMPA/kainate receptor-mediated) and slow (mGluR1-mediated) inward currents. Slow currents (IDHPG) are measured in cells perfused with bafilomycin A1. (Calibration bar: 100 pA, 2 sec.) (c) The average ratios of DISC charge transfer (filled), Δ noise SD (open), or IDHPG amplitude (gray) are plotted. The ratio reflects the value at t = 40 min/t = 20 min.