Figure 3: Origin and propagation properties of thalamic waves.

(a) Site of origin (colour-coded filled contours) and corresponding maximum spread (colour outlines) of five successive waves originated in the dLGN–VPM and eight waves in the MGv–VPM nuclei. The area covered by the waves in the dLGN–VPM example was 149.728 μm²±5.873 μm² and in the MGv–VPM example was 188.715 μm²±16.722 μm². Insets represent examples of the propagation of wave 1 (red) and wave 2 (blue) for each pair. The white contours show the pattern of spread of the wave front measured at 250 ms intervals. (b) Quantification of the percentage of waves depending on the origin at E16.5. The vast majority of waves are originated in the VPM (**P=0.004; Paired t-test; *P=0.016; Wilcoxon matched-pairs signed rank test). (c) Schemas representing the stochastic nature of the thalamic waves origins for each pair of nuclei (dLGN–VPM; n=40 sites in five independent experiments; MGv–VPM, n=67 sites in five independent experiments). (d) Effect of bath application of the voltage-dependent sodium channels blocker tetrodoxin (TTX, 1 μM) on the Ca²⁺ activity. TTX completely abolished the thalamic waves without substantially affecting the asynchronous activity or the clusters. (e) Quantification of Ca²⁺ dLGN–VPM waves frequency before and during TTX administration. (f) Dose-dependent response in waves per minute, after increasing the extracellular potassium concentration from 5 mM (control) to 12 mM. (g) Effect of bath application of the gap junction blocker carbenoxolone (50 μM) on the Ca²⁺ activity. The most noticeable effect is the reversible abolition of the synchronous waves. (h) Quantification of Ca²⁺ dLGN–VPM waves frequency before, during and after carbenoxolone administration. Graphs represent mean±s.e.m. Scale bars, 250 μm.