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Figure 1 | Journal of Neuroinflammation

Figure 1

From: Transient hypercapnia reveals an underlying cerebrovascular pathology in a murine model for HIV-1 associated neuroinflammation: role of NO-cGMP signaling and normalization by inhibition of cyclic nucleotide phosphodiesterase-5

Figure 1

Tat-transgenic mice display attenuated cerebrovascular response to hypercapnic challenge. (A) Cerebral blood flow (CBF) change in response to 5-minute exposure to 6% CO2, as measured by laser Doppler flowmetry (LDF). Results represent mean from seven Tat-transgenic (Tat-tg) mice and four wild type (WT) mice. (B) Maximum CBF reached in response to exposure to 6% CO2, for the data shown in (A). **P <0.01, nonparametric permutation test. (C) CBF change in response to 30-second exposure to 6% CO2, as measured by LDF. Results represent mean from five Tat-tg mice, four Tat-tg mice not induced with doxycycline (DOX) (Tat-tg UI) and five WT mice. (D) Maximum CBF reached in response to exposure to 6% CO2, for the data shown in (C). **P <0.01, nonparametric permutation test. (A, C) Values are expressed as a percentage change from baseline CBF, defined here as the mean CBF measured during the one-minute period immediately preceding delivery of CO2. Shadowed area along X-axis represents duration of hypercapnic challenge. All data represent mean ± SEM. (E) Confirmation of inducible Tat expression in the cortex of Tat-tg mice, as analyzed by RT-PCR. A 141-bp Tat-specific PCR product is shown in the upper panel and a control 480-bp GAPDH product is shown in the lower panel. DNA-free RNA samples were analyzed from a WT c57Bl mouse (negative control), two Tat-tg DOX+ mice, two Tat-tg DOX- mice; genomic DNA from a Tag-tg mouse was used as a positive control (gDNA Tat-tg)

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