Fig. 3. L-type Ca2+ channel agonists induce large, frequent, rapidly propagating waves of activity that persist in the presence of neurotransmitter antagonists that abolish control retinal waves. A, The evolution of individual retinal waves in control (left) and FPL-containing (right) conditions. Each color represents the wave area at time intervals of 1 sec, with the wave propagating fromred to green to blue.B, The time course of ΔF/F of fura-2 under control conditions (top left trace), after blockade of waves with DHβE (2 μm;top right trace), and in the presence of BayK and antagonists of AMPA–kainate (DNQX; 25 μm), NMDA (d-APV; 50 μm), GABAA (bicuculine methiodide; 10 μm), and glycine (strychnine; 2 μm) receptors (bottom trace), as indicated by theasterisk. C, ΔF/F averaged over a 200 μm2 area in a retina taken from a mouse lacking the β2 subunit of the nAChR under control conditions and after bath application of FPL (bottom trace).D, A whole-cell current-clamp recording from an RGC in control conditions (top left trace) and in the presence of DHβE (2 μm;top right trace).Bottom trace, current-clamp recording in the presence of FPL and the neurotransmitter antagonists listed above.E, Summary of the effects of L-type Ca2+ channel agonists on interwave (ΔF/F) or interburst (I-Clamp) intervals [for Control, L-type Ca2+channel agonist (Bay, FPL), and agonist + fast transmitter antagonist (+Antag.) conditions, respectively, n = 36, 16, and 23 retinas for ΔF/F; n = 37, 16, and 19 RGCs for current-clamp].