Figure 3.

Evidence of decreased glutamate subtype transporter-1 (GLT1) and increased caspase-3 activity in oligodendrocytes of cocaine-treated mice. A: GLT1 levels in NAc of control; 17 days ceftriaxone only (Ceft) followed by 30 days vehicle during withdrawal; 14 days cocaine only (Coc) followed by 30 days vehicle during withdrawal; 3 days Ceft pretreatment followed by 14 days of ceftriaxone and cocaine (Coc with Ceft) and 30 days of vehicle during withdrawal; 14 days of cocaine followed by 30 days ceftriaxone (Coc then Ceft) during withdrawal. *P < 0.01. B: Representative Western blot of GLT1 levels in 10 μg protein from NAc from one mouse from each group. GADPH was used as a loading control. C: Representative using Western blot of cleaved caspase-3 levels in 40 μg protein from NAc from one mouse from each group. GAPDH was used as a loading control. *P < 0.05, **P < 0.01. D: Cleaved caspase-3 protein levels in control; 14 days cocaine followed by 30 days vehicle during withdrawal (Coc); 14 days of cocaine followed by 30 days ceftriaxone during withdrawal (Coc then Ceft). n = 8 to 10 mice per group with one-way analysis of variance with Bonferroni's multiple comparison post-hoc testing. E–G: NAc tissues from representative mice are labeled with an antibody against cleaved caspase-3 in green, CC1, an oligodendrocyte-specific maker in red, and nuclei in blue with DAPI. E: NAc tissues from control show robust CC1-immunoreactivity (red) with no evidence of caspase-3 activity. F: NAc tissues from cocaine-treated mice show decreased CC1-immunoreactivity (red) with evidence of caspase-3 activity (green, arrowheads) associated with CC1-1+ oligodendrocytes (red). G: NAc tissues from cocaine treated mice that received ceftriaxone during withdrawal show CC1-immunoreactivity (red) with undetectable caspase-3 activity (green). Original magnification, ×100. Scale bar = 10 μm.