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. Author manuscript; available in PMC: 2018 Nov 29.
Published in final edited form as: Mol Psychiatry. 2017 Nov 28;23(10):2057–2065. doi: 10.1038/mp.2017.230

Figure 3.

Figure 3

The burst-firing mode of TRN neurons was impaired in GCLM KO mice in vitro. (a) and (b) Spiking pattern of spontaneously active TRN neurons was altered in GCLM KO mice. (a) Frequency of bursts. More TRN neurons did not burst in GCLM KO as compared to WT mice (p = 0.03; Mann-Whitney U test). (b) Frequency of tonic spikes. No significant difference in the tonic mode between both genotypes. Data are based on 26 and 43 recorded neurons in 4 WT and 4 KO mice, respectively. (c) Proportion of TRN neurons exhibiting a burst versus a tonic firing when kept at 4 different membrane potential levels. Note the significantly smaller number of neurons bursting at ~–70 mV in GCLM KO as compared to WT mice (total number of recorded neurons: 17 and 15 in WT and KO, respectively). * significantly different between genotypes (p = 0.015; Fisher exact test, p value corrected for multiple comparisons). The traces in the inset show a TRN neuron exhibiting a tonic (upper trace) and a bursting (lower trace) response upon a depolarization current while its membrane potential was at −61 and −71 mV, respectively. (d) The maximum number of action potentials generated within a single burst was significantly smaller in TRN neurons of KO as compared to WT mice (p = 0.009; ANOVA). (e) When the membrane potential was kept at ~−60mV, the tonic response to depolarization currents was not different between genotypes (number of neurons: 10 and 12 in WT and KO, respectively).