Figure 2.

Gadoteridol enhances rAAV5-mediated, but not rAAV2-mediated, distribution in rat striatum. (a) Left hemispheres were injected with AAV + lactated Ringer’s solution. Right hemispheres were injected with AAV + 2 mmol/l Gd. Similar results were observed with 1 mmol/l Gd (b–d). Scale bar = 1 mm. (b–d) Quantification of the effects of gadoteridol in the distribution of rAAV2 and rAAV5 by OD analysis. (b) Mean OD of GFP immunoreactivity. (c) Total area above threshold of GFP immunoreactivity and (d) ratio of volume of distribution versus volume of infusion of GFP immunoreactivity (in mm³/µl). (e) Gadoteridol does not affect tissue health. Left panel: Nissl staining reveals no cell damage outside of the needle track in both hemispheres. Immunostaining for markers of inflammation (middle panel: GFAP, a marker of activated astrocytes; right panel: CD-11b, a marker for activated microglia) show no inflammation in either hemisphere outside of the needle track area. High magnification insets show representative needle track inflammation and cell damage. For all figure panels in e, right hemispheres were injected with AAV + Gd and left hemispheres with AAV + lactated Ringer’s solution. Scale bar = 1 mm. Data (a,b,c,d) represent the mean ± SEM (AAV2 1 mmol/l Gd group, n = 6; AAV2 2 mmol/l Gd group, n = 5; AAV5 1 mmol/l Gd group, n = 5; AAV5 2mmol/l Gd group, n = 5). *P < 0.05; **P < 0.005; ***P < 0.0005. Significant indicators above histogram bars indicate comparison to control side (no contrast agent) within same treatment group. Gd, gadoteridol; GFP, green fluorescent protein; OD, optical density; rAAV, recombinant adeno-associated virus.