Fig. 2: Behavioural consequences of RtTg inactivation.
From: A Brainstem reticulotegmental neural ensemble drives acoustic startle reflexes
a Left: schematic for chemogenetic inactivation of RtTg neurons. Right: a representative image confirming hM4Di-mCherry expression. Scale bar, 300 μm. b Left: schematic for the ASR paradigm. Right: quantitative graph showing the effect of RtTg inactivation on ASR amplitudes (n = 8 per group; t = 2.417, P = 0.02 (85 dB); t = 3.429, P = 0.0014 (90 dB); t = 5.976, P = 4.3 × 10−7 (95 dB)). c Left: representative movement tracks of hM4Di-infected mice after i.p. injection of saline or CNO. Quantification of total distances (middle, n = 8 per group; P = 0.7637) and average speed (right, n = 8 per group; P = 0.6411) during open field test. d Representative images showing a mouse walking on treadmill and paw prints detected from a video settled under the treadmill. e–g Digi Gait analysis for hM4Di infected mice after i.p. injection of saline or CNO (n = 8 per group; for e: t = 0.2945, P = 0.7705 (fore limb); t = 0.1914, P = 0.8496 (hindlimb); for f: t = 0.2689, P = 0.7899 (fore limb); t = 0.4781, P = 0.6363 (hindlimb); for g: t = 0.9117, P = 0.3697 (fore limb); t = 0.4126, P = 0.6831 (hindlimb)). h Latency to fall on accelerating rotarod of hM4Di-infected mice after i.p. injection of saline or CNO (n = 8 per group; F = 0.2, P = 0.9346). i Tail-flick latency of hM4Di-infected mice after i.p. injection of saline or CNO (n = 8 per group, P = 0.8269). Error bar represent mean ± s.e.m. Significance was assessed using two-sided unpaired t-tests in c,i, and two-way ANOVA combining with FDR corrections in b, e–h. * P < 0.05; ** P < 0.01; *** P < 0.001; ns, not significant.
