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. 2013 Oct 15;21(12):2148–2159. doi: 10.1038/mt.2013.211

Figure 1.

Figure 1

AAV9 transduction pattern and persistence in SOD1G93A mice. SOD1G93A mice were injected intravenously with AAV9-CB-GFP at P1 and P21 and euthanized 21 days postinjection (n = 3 per time point). Spinal cords were examined for GFP, ChAT (motor neuron marker), and GFAP (astrocyte marker) expression. (a,f,k,p) Temporal vein injection of AAV9-CB-GFP at P1 resulted in efficient transduction of motor neurons and glia in SOD1G93A mice. (b,g,l,q) Tail vein injection at P21 predominantly targeted astrocytes with few GFP-positive motor neurons. To test the persistence of transduced cells, AAV9-CB-GFP was intravenously injected at P1 and P21 in SOD1G93A animals that were killed at end stage (~P130). (c,d,h,i,m,n,r,s) Immunofluorescence analysis of lumbar ventral horn demonstrated that GFP expression was maintained in astrocytes throughout the disease course. To determine whether SOD1-mediated inflammation and damage would affect AAV9 transduction, we intravenously injected SOD1G93A mice at P85 and harvested their spinal cords at end stage. There was no difference observed in the transduction pattern of SOD1G93A mice treated at P21 or P85. Insets in (r–t) show colocalization between GFP and GFAP signal. (u) Quantification of transduced cells in ALS spinal cords (for each group tissues were analyzed from three animals). GFP, ChAT,and GFAP columns show numbers of cells counted. Bars = 100 µm. AAV, adeno-associated virus; GFP, green fluorescent protein; ChAT, choline acetyltransferase; GFAP, glial fibrillary acidic protein; P1, postnatal day 1; P21, postnatal day 21; P85, postnatal day 85.