PMC

Detection of MOR and KOR opioid receptor transcripts by RT-PCR. MOR (A) or KOR (B) mRNA was not detected at 24 h, but was expressed at 5 DIV; GRPs (+) and blank lanes (−) lacking MOR or KOR mRNA, respectively.

Co-localization of μ (MOR), δ (DOR), and κ (KOR) opioid receptors with Sox2+ and Nkx2.2+ glial precursors at 2-3 DIV (A-I) and 5 DIV (J-P). Opioid receptors are widely expressed by subpopulations of Sox2+/Nkx2.2+ glial precursors (A-P). Note, MOR, Nkx2.2 and Sox2 immunoreactivity can be localized to the same cell (arrow in M-P) and overlapping Sox2 and Nkx2.2 immunoreactivity was evident in some DOR or KOR expressing cells (data not shown); scale bar = 20 μm (A,D,G); scale bar = 25 μm (B-C,E-F,H-I); scale bar = 10 μm (J-P).

Effects of morphine and/or Tat_1-72 on caspase 3 activity at 4 h (A) and on the proportion of cleaved caspase-3 immunoreactive GRPs at 24 h (B). Although morphine or Tat_1-72 increased caspase-3 activity at 4 h, the proportion of cleaved caspase-3 immunoreactive GRPs was unchanged at 24 h. Data represent (n=4) independent experiments performed on cells derived from separate litters cultured for 1 DIV. Values are mean fold-change from control ± SEM (*P < 0.05 vs. vehicle-treated control cultures).

Effects of opiates and/or Tat_1-72 (Tat), Tat_Δ31-61 [(mut)Tat], or immunoneutralized Tat [(neutr)Tat] on the viability of glial precursors after 24 h (A) or 96 h (B) of continuous exposure. Both morphine (Morph) and Tat_1-72 alone caused significant increases in the proportion of dying, ethidium monoxide-positive (EMA⁺) glial precursors (*P < 0.05 vs. vehicle-treated controls), while (neutr)Tat and (mut)Tat did not increase the percentage of EMA⁺ cells (^#P < 0.05 vs. treatment with Tat_1-72). In combination, morphine and Tat_1-72 did not increase the proportion of EMA⁺ cells beyond the rate of death seen with either substance alone. In the presence of the MOR selective antagonist β-funaltrexamine (FNA), morphine did not cause significant increases in cell death. Values are the mean ± SEM fold-change in EMA⁺ cells compared to vehicle-treated controls from 4-11 experiments initiated at 1 DIV.