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. Author manuscript; available in PMC: 2009 Nov 10.
Published in final edited form as: J Comp Neurol. 2008 Nov 10;511(2):271–285. doi: 10.1002/cne.21835

Fig. 3.

Fig. 3

MAP2, αII-spectrin, total cell counts and cortical thickness are all unchanged in mPFC of D1-primed rats. (A) Representative Western blot of MAP2 and β-actin in mPFC of SKF-38393-treated sham (Sham-SKF) and lesioned rats (Les-SKF) and their saline-treated counterparts (Sham-Sal and Les-Sal, respectively). Faint bands in the center of each lane are consistent with MAP2 degradation products. (B) Spectrin and its breakdown products (SBDPs) in mPFC homogenates from Sham-Sal and Les-SKF rats. Neither the 145-150 kDa calpain-mediated cleavage products, nor the 120 kDa caspase-3 SBDP were altered by D1 priming. (C) Cresyl violet-stained neurons counted at day 21 after dosing across superficial (I-III) and deep (V-VI) mPFC layers. Data are expressed as percent of total cell counts across all layers: black bars, Sham-Sal, 4810.5 ± 130.7 total cells; dark gray bars, Sham-SKF, 4237.7 ± 289.2 cells; white bars, Les-Sal, 4781.0 ± 441.9 cells; light gray bars, Les-SKF, 4326.5 ± 269.2 cells counted across all layers. (D) Mean cortical layer thickness at day 21 plotted as percent of total mPFC thickness. Filled squares, Sham-Sal; filled circles, Sham-SKF; open squares, Les-Sal; open circles, Les-SKF.