Figure 6: EGFL7 altered neurogenesis and behaviour.

(a) Experimental set-up. (b–d) Ectopic EGFL7 increased the amount of adult-born neurons (IF; 229.8±7.56 versus 176.7±7.14 cells per mm in AdMock; n=6; P<0.005), while (e–g) less neurons were detected in the OB of EGFL7−/− (135.9±21.79 versus 274.6±28.35 cells per mm in WT; n=6; P<0.005) or (h) EGFL7iΔNSC mice (242.0±42.37 versus 424.3±18.68 cells per mm in WT; n=3; P<0.05). (i,j) Electrophysiological conduction from mitral cells in the OB of EGFL7−/− mice revealed (i) an increase in the average evoked firing rate of EGFL7−/− mice upon amyl acetate exposure (8.55±1.17 versus 6.41±0.66% in WT; n(WT)=53, n(EGFL7−/−)=43; P<0.05). (j) Comparison of the proportions of synchronous (black boxes) and asynchronous firing neurons (white boxes) or other interacting neurons (grey boxes) upon exposure to amyl acetate revealed a majority of asynchronous firing (46±13 versus 26±14% in WT; P<0.05; n(WT)=53, n(EGFL7−/−)=43) in EGFL7−/− mice but synchronous firing in WT (37±15 versus 63±19% in WT; P<0.05; n(WT)=53, n(EGFL7−/−)=43). (k,l) EGFL7−/− mice displayed a deficit in olfactory preference for both (k) artificial (water/vanilla; 3.53±2.16 versus 6.03±4.23 s in WT; n=12; F(2, 56)=4.047, P<0.05, two-way ANOVA for repeated measures) and (l) natural (water/male urine; 6.0±3.42 versus 10.53±7.35 s in WT; n=12; F(2, 50)=5.891, P=0.005, two-way ANOVA for repeated measures) scents. (m,n) EGFL7−/− mice displayed elevated tolerance to (m) 2-MB (79.49±81.3 versus 20.1±23.73% in WT; n=20; F(6, 282)=2.319, P<0.05, two-way ANOVA for repeated measures) and (n) TMT (116.36±99.25 versus 56.36±55.13% in WT; n=13; F(1, 18)=7.351, P<0.05, two-way ANOVA for repeated measures) in olfactory avoidance tests. Data suggest loss of EGFL7 impaired olfactory perception. Scale bar, 50 μm (b,c,e,f).