Fig. 6: Absence of developmental shift of the GABAAR-mediated response and of cortico-striatal GABAergic pause response after early chronic treatment of pups with the NKCC1 blocker bumetanide. | Communications Biology

Fig. 6: Absence of developmental shift of the GABAAR-mediated response and of cortico-striatal GABAergic pause response after early chronic treatment of pups with the NKCC1 blocker bumetanide.

From: The early excitatory action of striatal cholinergic-GABAergic microcircuits conditions the subsequent GABA inhibitory shift

Fig. 6

a, b Representative cell-attached recordings, and corresponding mean frequency histograms of the effect of isoguvacine (10 μM) on a P13 CGIN ongoing activity in slices from bumetanide (a) or vehicle (b) treated pups (see methods). c (top) Experimental protocol: cortical stimulation (20 Hz, 7 stimuli); c. d (left), representative cell-attached, superimposed (n = 15), consecutive responses to cortical train stimulation of P12- P14 CGIN in slices from bumetanide-treated mice (d) and vehicle (c) and mean frequency histograms. Note the absence of the pause response (d). c, d (right), Responses within the train at extended time scale to show the efficacy of cortical stimulation. e Quantification of data shown in (a, b) (bumetanide-treated: n = 16 cells (N = 3); vehicle-treated: n = 17 cells (N = 3). f, g Quantification of data shown in (c, d): mean number of spikes during two different time windows after cortical train stimulation (0–500 ms, 0–1400 ms) normalized to spikes counts before the train (bumetanide-treated: n = 7 cells (N = 3); vehicle-treated: n = 10 cells (N = 3)). All means ± s.e.m (Supplementary Table 15). n = number of cells, N = number of mice.

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