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Table 2 Effects of Tat and morphine on microglial morphology in the striatum and spinal cord of Tat transgenic mice

From: Escalating morphine dosing in HIV-1 Tat transgenic mice with sustained Tat exposure reveals an allostatic shift in neuroinflammatory regulation accompanied by increased neuroprotective non-endocannabinoid lipid signaling molecules and amino acids

CNS region Measure Genotype Repeated saline Repeated morphine Genotype effect Drug effect Genotype x drug
    mean ± SEM mean ± SEM F1, 56 p F1, 56 p F1, 56 p
Striatum Soma area (μm2) Tat(−) 51.1 ± 2.16 46.7 ± 2.98 < 1.0 0.49 2.9 0.09 < 1.0 0.96
Tat(+) 49.2 ± 2.41 45.1 ± 2.00
Maximum branch length (μm) Tat(−) 35.3 ± 3.32 32.5 ± 2.59 < 1.0 0.59 < 1.0 0.84 1.7 0.20
Tat(+) 30.7 ± 1.90 34.4 ± 2.19
Critical radius (μm) Tat(−) 14.6 ± 1.56 13.4 ± 1.35 < 1.0 0.51 < 1.0 0.97 < 1.0 0.63
Tat(+) 14.4 ± 1.76 15.6 ± 1.20
Number of primary process Tat(−) 4.8 ± 0.56 4.1 ± 0.30 2.8 0.10 < 1.0 0.92 2.8 0.10
Tat(+) 3.5 ± 0.29 4.1 ± 0.45
Process maximum Tat(−) 6.8 ± 0.83 5.3 ± 0.60 < 1.0 0.93 < 1.0 0.70 2.3 0.13
Tat(+) 5.5 ± 1.00 6.4 ± 0.77
Process total Tat(−) 21.5 ± 3.02 16.1 ± 2.20 < 1.0 0.89 < 1.0 0.70 2.1 0.16
Tat(+) 16.9 ± 3.49 19.9 ± 2.77
Spinal cord Soma area (μm2) Tat(−) 48.5 ± 3.42 50.9 ± 3.79 4.2 0.04 3.8 0.06 1.5 0.23
Tat(+) 51.4 ± 2.45 62.2 ± 3.73
Maximum branch length (μm) Tat(−) 35.1 ± 2.59 36.2 ± 2.71 < 1.0 0.51 < 1.0 0.66 < 1.0 0.98
Tat(+) 33.4 ± 2.32 34.6 ± 2.19
Critical radius (μm) Tat(−) 16.7 ± 1.98 15.6 ± 1.20 < 1.0 0.44 < 1.0 0.98 < 1.0 0.61
Tat(+) 17.2 ± 2.28 18.1 ± 2.04
Number of primary process Tat(−) 2.3 ± 0.28 2.7 ± 0.33 < 1.0 0.81 1.5 0.23 5.0 0.03
Tat(+) 3.2 ± 0.47 2.0 ± 0.20
Process maximum Tat(−) 3.6 ± 0.31 4.6 ± 0.57 < 1.0 0.81 < 1.0 0.78 5.4 0.02
Tat(+) 4.8 ± 0.58 3.6 ± 0.27
Process total Tat(−) 11.5 ± 1.56 15.7 ± 2.30 < 1.0 0.58 < 1.0 0.95 5.1 0.03
Tat(+) 14.6 ± 1.75 10.6 ± 1.22
  1. Sholl analysis of microglial morphology in the striatum and spinal cord of repeated (8-day) saline- or morphine-treated Tat(−) and Tat(+) mice. Data are expressed as the mean ± SEM. The parameters measured by Sholl analysis are indicated in parentheses in the second column. One-way ANOVAs for each CNS region were conducted with genotype and drug as between-subjects factors. F values and p values are presented from ANOVA results. Bolded values denote significant differences at α = 0.05; mean ± SEM, n = 3–4 mice per group/4 sections each