Differential Regulation of Intracisternally Injected Angiotensin II-Induced Mechanical Allodynia and Thermal Hyperalgesia in Rats

Figures

• 

  Figure 1. Changes in air-puff thresholds and head-withdrawal latency after intracisternal Ang II injection. (A) Intracisternally-injected Ang II (0.1, 0.5, or 2.5 ng) significantly decreased air puff thresholds. Intracisternal vehicle injection did not affect air puff threshold. (B) Intracisternal injection of high-dose Ang II (2.5 ng) also significantly decreased head withdrawal latency. Neither low-dose Ang II nor vehicle affected head withdrawal latency. * p < 0.05, vehicle vs. Ang II-treated group, n = 7 animals/group.

• 

  Figure 2. Effects of angiotensin II receptor antagonists on intracisternally injected Ang II-induced mechanical allodynia and thermal hyperalgesia. (A) Intracisternal injection of AT1R antagonist losartan (20 μg) blocked Ang II-induced mechanical allodynia. Neither low-dose losartan nor vehicle affected air-puff thresholds. (B) Losartan injection did not affect thermal hyperalgesia. (C) Intracisternal administration of AT2R antagonist PD123319 did not affect Ang II-induced mechanical allodynia. (D) Both doses of PD123319 (150 and 300 μg) significantly decreased thermal hyperalgesia compared with vehicle. * p < 0.05, vehicle vs. AT1/2 receptor-antagonist-treated group, n = 7 animals/group.

• 

  Figure 3. Characterization of AT1R and AT2R in the ipsilateral trigeminal subnucleus caudalis and trigeminal ganglion. (A) Double immunofluorescence analysis for AT1R (red) with astrocyte marker (GFAP), microglial marker (Iba1), and neuronal marker (NeuN). AT1R immunoreactive cells were found to mainly be colocalized with GFAP. (B) Double immunofluorescence analysis for AT2R (red) colocalized with c-terminal marker (CGRP). AT2R colocalized with CGRP in the ipsilateral trigeminal subnucleus caudalis. (C) Double immunofluorescence staining for AT2R (red) with CGRP-positive neurons in the trigeminal ganglion. AT2R colocalized with CGRP-positive neurons in the trigeminal ganglion. Scale bar, 50 μm.

• 

  Figure 4. Effects of glial cell inhibition on Ang II-induced mechanical allodynia. (A) Pretreatment with minocycline (50, 100 μg), a microglial inhibitor, did not affect air puff thresholds. (B) Intracisternal pretreatment with LAA (8 μg), an astrocyte inhibitor, significantly inhibited Ang II-induced mechanical allodynia. * p < 0.05, vehicle vs. LAA-treated group, n = 7 animals/group.

• 

  Figure 5. Effects of botulinum toxin type A on Ang II-induced mechanical allodynia and thermal hyperalgesia. (A) Pretreatment with BTX-A did not affect Ang II-induced mechanical allodynia. (B) Pretreatment with BTX-A significantly inhibited Ang II-induced thermal hyperalgesia. * p < 0.05, vehicle vs. BTX-A-treated group, n = 7 animals/group.