Skip to main content
. Author manuscript; available in PMC: 2015 Jan 27.
Published in final edited form as: Neuroscience. 2007 May 2;146(4):1546–1554. doi: 10.1016/j.neuroscience.2007.03.006

Fig. 4.

Fig. 4

Effects of opiates and/or Tat1-72 (Tat), TatΔ31-61 [(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 Tat1-72 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 Tat1-72). In combination, morphine and Tat1-72 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.