Fig. 4: Chronic haloperidol administration does not affect SV2A levels in the rat frontal cortex (FC).

a Example of western blots showing total SV2A levels in synaptosomes isolated from the FC. b Quantification of total SV2A levels on western blot, normalised to GAPDH, showed no significant changes upon chronic haloperidol treatment (Kruskal–Wallis test, p = 0.71). c Autoradiography images of brain sections incubated with 12.5 nM [³H]UCB-J in absence (left) or presence (right) of levetiracetam (a drug that binds to SV2A). Black boxes indicate which ROI was selected to measure tracer binding in the prefrontal cortex, PFC (top), or anterior cingulate cortex, ACC (bottom). WM, white matter. Colour bar indicates [³H]UCB-J binding levels. Scale bar, 1 mm d Quantification of [³H]UCB-J binding in PFC (top) and ACC (bottom), indicating no significant changes upon chronic haloperidol treatment (two-way ANOVA, F_2,12 = 1.451, p = 0.27). e Top: schematic of brain section at Bregma 1.1 mm. Bottom: low magnification fluorescent image of a rat brain section immunostained for SV2A (red) and DAPI (blue). Scale bar, 250 µm. ACC, anterior cingulate cortex; WM, white matter; STR, striatum. f High-magnification confocal images of brain sections from vehicle- (top) or haloperidol- (bottom) treated animals, showing punctate immunostaining for SV2A. Both raw images (left hand side) as well as background corrected images (right hand side) are shown. White arrows indicate a lack of SV2A punctae in the cell body; yellow arrows indicate examples of presynaptic terminals at perisomatic synapses and proximal dendrites. Scale bar, 10 µm (large field of view) or 4 µm (zoomed insets). g Quantification of background corrected SV2A intensity values. There were no significant differences in SV2A immunostaining intensity between vehicle- and haloperidol-treated groups (two-way ANOVA with Bonferroni’s multiple comparison correction, F_1,20 = 0.1412, p = 0.71). Error bars indicate standard error of the mean.