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. 2022 Jun 15;5:589. doi: 10.1038/s42003-022-03446-1

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a Locomotor response to acute amphetamine (2.5 mg/kg) challenge after considering differences in baseline locomotion. Compared with the respective saline-treated groups, amphetamine significantly increased locomotor activity in Mkln1^+/+ mice (left panel) but had negligible effect in Mkln1^–/– mice (right panel; genotype × drug × time bins: (F(23,1518) = 2.23, P < 0.01). Restricted analyses to each genotype groups revealed a pronounced drug effect in Mkln1^+/+ mice (drug × time bins: F(23,782) = 3.20, P < 0.0001) followed by Bonferroni post hoc test for pairwise comparisons (*P < 0.05, **P < 0.01) but not in the Mkln1^–/– group. b Overall, Mkln1^–/– mice showed significantly diminished locomotor response to amphetamine compared with Mkln1^+/+ controls (genotype: F(1,66) = 5.47, P < 0.05) followed by Bonferroni post hoc test for pairwise comparisons (*P < 0.05). c Both Mkln1^–/– and Mkln1^+/+ mouse groups show a comparable increase in startle reactivity in response to pulse stimuli of increasing sound intensity (dB intensity: F(9,144) = 65.82, P < 0.0001). d, e The absence of muskelin did not affect startle response to pulse-alone (d) and prepulse-alone (e) stimuli. f Percent PPI depicted as function of increasing prepulse intensities for each pulse intensity (prepulse intensities: +6, +12, and +18 dB above background (65 dB) noise). Mkln1^–/– mice show highly similar PPI levels as Mkln1^+/+ controls (prepulse: F(2,52) = 149.17, P < 0.0001). g Habituation of startle responses following the presentation of 120 dB acoustic stimuli. Each block comprises 5 trials of acoustic stimuli. Both genotypes show a decline in the response amplitude as a function of trials (trial: F(9,153) = 3.14, P < 0.01). For data related to a, b (Amph: Mkln1^+/+ (N = 21: M = 10, F = 11); Mkln1^–/– (N = 18: M = 7, F = 11); Saline: Mkln1^+/+ (N = 17: M = 8, F = 9); Mkln1^–/– (N = 18: M = 8, F = 10); c (Mkln1^+/+ (N = 10: M = 5, F = 5); Mkln1^–/– (N = 10: M = 5, F = 5); d–f (Mkln1^+/+ (N = 15: M = 8, F = 7); Mkln1^–/– (N = 15: M = 8, F = 7); g (Mkln1^+/+ (N = 11: M = 5, F = 6); Mkln1^–/– (N = 10: M = 5, F = 5). Data are presented as means ± SEM.