Figure 1 : Brain targeted knock-down of SPL and its impact on sphingolipid content and behaviour.

From: Sphingosine 1-phosphate lyase ablation disrupts presynaptic architecture and function via an ubiquitin- proteasome mediated mechanism

Figure 1

SPL expression was assessed in the indicated brain domains of 6 weeks old mice of the indicated genotype by (a) qRT-PCR (unpaired t-test, P < 0.0001) (b) Western blotting and quantification (unpaired t-test, P < 0.0001) as described in the Methods section (c) Sphingolipids from the cerebellum and the hippocampus of mice at the indicated age and genotype were determined by LC/MS/MS as described in the Methods section. Sphingosine 1-phosphate (S1P) and sphingosine (Sph) increased considerably already after 9 weeks in brains of SPLfl/fl/Nes but not SPLfl/fl/CaMK mice. Bars represent means ± SEM (n ≥ 3; two-way ANOVA, PS1P,h6w = 0.041, PS1P,h12m = 0.0458, PS1P,c6w = 0.041, PS1P,c12m = 0.0458, PSph,h6w = 0.0326, PSph,h12m = 0.0284, PSph,c6w = 0.0326, PSph,c12m = 0.0284). The amount of all other lipids determined including ceramides did not change upon SPL knockdown (not shown). (d) Open field test: exploratory locomotor activity is expressed as the distance covered during 20 min. (e), Object placement recognition test: shown is the exploration time of the objects in the novel and familiar location (two-way ANOVA, P = 0.0265) and the discrimination index, represented by the normalized ratio of time spent with the object placed in the novel area and the object in the familiar area (unpaired t-test, P = 0.0097). (f) Latency to fall from the accelerating rotarod (two-way ANOVA, P < 0.0001).