Fig. 2: Limited role of direct neuromodulatory inputs for spontaneous movement-dependent neuronal activity in wS1.
From: Brain-wide presynaptic networks of functionally distinct cortical neurons
a, Experimental approach for local delivery of receptor blockers during two-photon Ca2+ imaging. Triangles, PNs (GCaMP6+); circles, GABAergic neurons. Scale bar, 0.3 mm. b–d, Activity of an example Movup neuron during spontaneous movements before and after blockade of ACh (atropine and mecamylamine; b), noradrenaline (prazosin and propranolol; c), NMDA (d-2-amino-5-phosphonovaleric acid (d-AP5); d), or NMDA and AMPA (Glu, d-AP5 and 6,7-dinitroquinoxaline-2,3-dione (DNQX); d) receptors. Black, fluorescence traces; cyan, whisker movements. e–h, Correlation (r) between the activity of individual neurons and whisker movements during ACh (n = 1,300, 6 FOVs, 6 mice; e), noradrenaline (n = 1,483, 6 FOVs, 6 mice; f), NMDA (n = 720, 5 FOVs, 5 mice; g) or Glu (n = 956, 6 FOVs; 6 mice, h) receptor blockade versus baseline, respectively; sham sessions (Ringer’s only versus baseline) are included in e–h (cyan, n = 1,597, 5 FOVs, 3 mice) (null hypothesis, equal slopes: ACh receptor versus sham, P = 0.033; noradrenaline receptor versus sham, P = 0.13; NMDA receptor versus sham, P < 0.0001; Glu receptor versus sham, P < 0.0001; multiple comparisons with Bonferroni correction). i, Prediction of whisker movements from population activity. Out-of-sample R2 ratio (ACh receptor versus sham, P = 0.33; noradrenaline receptor versus sham, P > 0.05; NMDA receptor versus sham, P = 0.032; Glu receptor versus sham, P = 0.017; NMDA receptor versus Glu receptor, P < 0.0001; Kruskal–Wallis test (P = 0.00022) followed by two-sided Wilcoxon rank-sum tests with Bonferroni correction; n as in e–h). In box plots, the central line and box represent the median and 25th–75th percentiles, and whiskers extend to the most extreme data points excluding outliers (larger than 1.5× the interquartile range).
