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Results: 6

1.
Figure 1

Figure 1. Inactivation of Six5 or Dmpk does not affect anxiety or general motor activity in the Open Field task.. From: Muscleblind1, but Not Dmpk or Six5, Contributes to a Complex Phenotype of Muscular and Motivational Deficits in Mouse Models of Myotonic Dystrophy.

Anxiety, as indicated by thigmotaxis, is shown as % time hugging wall (panels i). Activity is shown as velocity (cm/s, panels ii) and ambulation (m traveled, panels iii). A) Six5−/− (white, n = 7) mutant mice display normal thigmotaxis, velocity and distance travelled compared to their Six5+/+ wild-type littermate controls, (black, n = 6) (panel i, ii, and iii respectively). B) Dmpk−/− mutant mice (white, n = 9) display normal thigmotaxis, velocity and distance travelled compared to their Dmpk+/+ wild-type littermate controls, (black, n = 9) (panel i, ii and iii, respectively). C) Mbnl1−/− (white, n = 23) mutant mice display increased thigmotaxis (F(1, 04) = 10.3, p = 0.0026), decreased velocity (F(1,40) = 14.0, p = 0.0006) and decreased distance travelled (F(1,40) = 8.10, p = 0.0070) compared to their Mbnl1+/+ wild type littermate controls (black, n = 19) (panel i, ii and iii, respectively).

Anna Matynia, et al. PLoS One. 2010;5(3):e9857.
2.
Figure 5

Figure 5. All three mutant mouse strains have normal spatial memory in the Morris Water Maze.. From: Muscleblind1, but Not Dmpk or Six5, Contributes to a Complex Phenotype of Muscular and Motivational Deficits in Mouse Models of Myotonic Dystrophy.

The percent time spent in the Target Quadrant (TQ), Adjacent Left (AL), Adjacent Right (AR) or Opposite Quadrant (OP) is shown. A score of 25% reflects random searching. Probe test results after training are shown. A) No differences were found in the percent time spent in the searching in each quadrant on day 7 as shown for Six5+/+ (black, n = 6) and Six5−/− (white, n = 7) mice. B) The percent time spent searching in each quadrant on day 7 is shown for Dmpk+/+ (black, n = 9) and Dmpk−/− (white, n = 9) mice. C) No differences were found in the percent time spent in searching in each quadrant on day 13 as shown for Mbnl1+/+ (black, n = 24) and Mbnl1−/− (white, n = 13) mice (genotype x quadrant, repeated measures ANOVA F(3,105) = 2.20, p = 0.092).

Anna Matynia, et al. PLoS One. 2010;5(3):e9857.
3.
Figure 6

Figure 6. Inactivation of Mbnl1 results in decreased sucrose consumption, a measure of motivation.. From: Muscleblind1, but Not Dmpk or Six5, Contributes to a Complex Phenotype of Muscular and Motivational Deficits in Mouse Models of Myotonic Dystrophy.

A) Mbnl1−/− (white, n = 14) mutant mice consume the same amount of water during habituation (0%) as well as during presentation of sucrose (2, 4, 8 and 16%) (genotype x water, repeated measures ANOVA F(4,104) = 1.67, p = 0.16) main effect of genotype (F(1,26) = 2.64, p = 0.12) compared to their wild-type littermate controls (black, n = 14). B) In contrast, Mbnl1−/− mutant mice consume less sucrose, regardless of the percent sucrose (genotype x sucrose, repeated measures ANOVA F(3,78) = 3.79, p = 0.014) main effect of genotype (F(1,26) = 6.23, p = 0.018). The Mbnl1−/− mutant mice drink less 2% (ANOVA F(1,26) = 4.96, p = 0.035), 4% (ANOVA F(1,26) = 4.46, p = 0.044), and 8% (ANOVA F(1,26) = 7.71, p = 0.010) sucrose but statistically consume the same amount of 16% (ANOVA F(1,26) = 3.00, p = 0.095) sucrose as their wild-type littermates, indicating that the mutant mice can taste and discriminate between water and the sweet solution.

Anna Matynia, et al. PLoS One. 2010;5(3):e9857.
4.
Figure 2

Figure 2. Inactivation of Mbnl1 does not alter anxiety in the Elevate Plus Maze.. From: Muscleblind1, but Not Dmpk or Six5, Contributes to a Complex Phenotype of Muscular and Motivational Deficits in Mouse Models of Myotonic Dystrophy.

A) Mbnl1−/− (white, n = 14) mutant mice spent the same amount of time in the open (F(1,26) = 0.76, p = 0.39) and closed arms (F(1,26) = 0.40, p = 0.53), and the center (F(1,26) = 0.52, p = 0.48) of the elevated plus maze compared to their Mbnl1+/+ wild type littermate controls (black, n = 14) (panel i, ii and iii, respectively), although the Mbnl1−/− mice show trends towards decreased anxiety by spending more time in the open arms. B) Mbnl1−/− mutant mice spent the significantly less time in a stretch posture, indicative of decreased anxiety (F(1,26) = 23, p<0.0001) C) Mbnl1−/− (white, n = 14) mutant mice display decreased overall activity, specifically decreased total entries into arms (F(1,26) = 8.4, p = 0.0076) which is due to decreased entries into the closed arms (F(1,26) = 9.4, p = 0.005) and not into open arms (F(1,26) = 3.6, p = 0.069) and compared to their Mbnl1+/+ wild type littermate controls (black, n = 14) (panel i, ii and iii, respectively). D) Mbnl1−/− (white, n = 14) mutant mice display decreased numbers of head dips (F(1,26) = 5.1, p = 0.032) compared to their Mbnl1+/+ wild type littermate controls (black, n = 14), incidcative of increased anxiety, in contrast to B).

Anna Matynia, et al. PLoS One. 2010;5(3):e9857.
5.
Figure 3

Figure 3. Inactivation of Six5, Dmpk or Mbnl1 does not affect Pavlovian contextual fear conditioning.. From: Muscleblind1, but Not Dmpk or Six5, Contributes to a Complex Phenotype of Muscular and Motivational Deficits in Mouse Models of Myotonic Dystrophy.

The percent time freezing (panels i) and the activity suppression ratios (a ratio of locomotor activity levels which corrects for hyper- and hypo-activity, panels ii) are shown for baseline (bl) and 7-day (7 d) memory of context fear conditioning. Baseline activity levels (arbitrary units) prior to the foot shock (panels iii) and activity bursts (velocity, cm/s, panels iv) are shown. A) Six5−/− (white, n = 7) mutant mice display no differences in context fear conditioning freezing, activity suppression, activity level or activity burst phenotypes compared to the Six5+/+ wild type littermate controls (black, n = 6). B) Dmpk−/− (white, n = 9) mutant mice display no differences in context fear conditioning freezing, activity suppression, activity level or activity burst phenotypes compared to the Dmpk+/+ wild-type littermate controls (black, n = 9). C) Mbnl1−/− (white, n = ) mutant mice display no context fear conditioning phenotype compared to their Mbnl1+/+ wild-type littermate controls (black, panels i and ii). However, Mbnl1−/− (white) mutant mice show decreased baseline activity compared to their Mbnl1+/+ wild type controls (black, panel iii) (F(1,14) = 6.86, p = 0.020). Mbnl1−/− (white, n = 5) mice also display a deficit in their unconditioned response to foot shock (activity burst) compared to their wild type controls (black, n = 12, panel iv) (effect of activity burst x genotype, repeated measures ANOVA F(1,14) = 15, p = 0.0018).

Anna Matynia, et al. PLoS One. 2010;5(3):e9857.
6.
Figure 4

Figure 4. Mbnl1−/− mutant mice have altered acquisition in the Morris Water Maze.. From: Muscleblind1, but Not Dmpk or Six5, Contributes to a Complex Phenotype of Muscular and Motivational Deficits in Mouse Models of Myotonic Dystrophy.

A) No differences were found in the latency (seconds) to find the platform during training (panel i), average velocity (cm/s) during all training days (panel ii) and thigmotaxis (F(1,23) = 2.8, p = 0.11) (% time, panel iii) for Six5−/− mice (white, n = 7) compared to their wild-type littermate controls, Six5+/+ mice (black, n = 6). B) No differences were found in the latency (seconds) to find the platform during training (panel i), average velocity (cm/s) during all training days (panel ii) and thigmotaxis (% time, panel iii) for Dmpk−/− mice (white, n = 9) compared to their wild-type littermate controls, Dmpk+/+ mice (black, n = 9). C) No statistical differences were found in the latency (seconds) to find the platform during training (panel i) (effect of genotype x latency using 2-day blocks, repeated measures ANOVA, F(6,210) = 1.19, p = 0.31) for Mbnl1−/− mice (white, n = 13) compared to their wild-type littermate controls, Mbnl1+/+ mice (black, n = 24). C inset: The pathlength (m) to reach the target platform of Mbnl1−/− (white) was the same as Mbnl1+/+ mice (black) during acquisition (effect of genotype x latency F(6,210) = 1.92, p = 0.080). In contrast, Mbnl1−/− mutant mice (white) had a slower average velocity during all training days (cm/s, panel ii) (F(1,35) = 38.5, p = <0.0001) and increased thigmotaxis (% time, panel iii) (F(1,35) = 6.47, p = 0.015) compared to their wild-type littermate controls, Mbnl1+/+ mice (black). D) The % time spent swimming slowly (floating behavior) of Mbnl1−/− (white) increased compared to Mbnl1+/+ mice (black) during acquisition (F(1,35) = 15.7, p = 0.0004; effect of genotype x latency F(6,210) = 6.53, p = <0.0001). Mbnl1−/− mice showed increased floating behavior in all training blocks except blocks 1 and 3. E) Mbnl1−/− mice (white) displayed normal acquisition in the visible water maze task (pathlength (m), (effect of genotype x pathlength using 2-day blocks, repeated measures ANOVA, F(6,70) = 0.885, p = 0.42)). Training blocks represent 1 day (2 training trials) for both Six5−/− and Dmpk−/− mutant mice, and two days (4 training trials) for Mbnl1−/− mutant mice. Mbnl1−/− and Mbnl+/+ mice exhibiting >10% thigmotaxis on the last day of training were excluded from these analyses. See Figure S1 for data including all Mbnl1 mice.

Anna Matynia, et al. PLoS One. 2010;5(3):e9857.

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