Sentence examples for mean spine density from inspiring English sources

In contrast, the mean spine density values in the distal dendritic domain of treated and control slices were not significantly different (P>0.6 for both 2 and 24 hours, Student's t-test) (Table 1A, Fig. 1B).

Both at 2 and 24 hours of treatment the mean spine density values in the treated slices were significantly higher relative to controls fixed at the same experimental time periods (P<0.001 in both cases, Student's t-test).

In GFP-wt and GFP-ho mice, the mean spine density, expressed as the number of spines per square micrometer (µm2) of dendritic surface, was 4.95 (±0.062 SE) and 4.11 (±0.18 SE), respectively.

It is clear that the dendrites of F-ERF neurons have higher spine density than S-ERF neurons, especially at the proximal segments of dendrites (20, 40, 60 µm levels from cell body, t-test, P<0.01). Figure 3D shows a comparison of mean spine density between the F-ERF and S-ERF cells.

Overall, we found a reduction in the mean spine density of P301S Tau mice by 17% (0.34 ± 0.04 compared to 0.41 ± 0.01 spines/μm in wildtype mice, Figure  1d).

Similar to Per2Brdm1, also Cry2−/− mice displayed a mean vertebral spine density (BV/TV) of 21.6±1.5% (mean±SD) in comparison to wild type (10.9±1.9%; Figure 3A).

Spine density (spine number/10 µm) measures were obtained for each dendrite and averaged within mice. Figure 2 presents mean dendritic spine density in CA1 pyramidal layer and dentate molecular layer for ephrin-A2 -/- and wildtype mice, contrasting rTMS to sham.

(B ) Quantification of dendritic spine density for conditions shown in A. Values are represented as mean ± SEM from 3 to 4 mice per genotype (for details on spine quantification see Table 1 ).

(F ) Quantification of dendritic spine density of GCs shown in E. Values are represented as mean ± SEM from 3 to 4 mice per genotype (for details on spine quantification see Table 1 ).

(B ) Spine density per 10 μm dendritic length from multiple neurons from A (mean ± SEM: control vector: 5.38 ± 0.48 spines; LIMK1 shRNA: 3.23 ± 0.15 spines; shRNA plus shr-wt-LIMK1: 4.99 ± 0.41 spines; shRNA plus shr-CCSS-LIMK1: 3.82 ± 0.40 spines; *p < 0.05 compared to control vector, ANOVA, Dunnett's post hoc correction. N = 40 50 neurons per condition).

The higher protrusion density observed in the midazolam group was associated with a significant decrease in mean spine head diameter (0.62±0.03 µm, control vs 0.41±0.01 µm, mida, P<0.001 Fig. 1c).