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Figure 1 | Molecular Pain

Figure 1

From: Genetic enhancement of neuropathic and inflammatory pain by forebrain upregulation of CREB-mediated transcription

Figure 1

Behavioral assessment of acute, inflammatory, and neuropathic pain. A) Acute nociception was unaltered by forebrain CREB overexpression. Response latencies in the hot plate and B) tail flick tests were similar between groups. C) 50% mechanical threshold levels were indistinguishable between groups. D) Formalin test, Y134F mice show significantly less licking responses than WT mice (F (1, 22) = 12.68, P = 0.004). E) A significant interaction was detected, whereby Y134F mice only showed decreases in Phase 2 (10 – 60 min) and 3 (60 – 120 min), but not Phase 1 (0 – 10 min) of the formalin test. Phase 1 corresponds with acute inflammatory pain, whereas Phase 2 and 3 represent more tonic states of pain. F) In the CFA model of chronic inflammatory pain, Y134F mice showed a significant enhancement in CFA induced mechanical allodynia up to 1 Week post CFA application (F (1, 18) = 21.67, P = 0.003). G) Enhanced allodynia was also seen in the uninjected paw. H) In the neuropathic pain model, Y134F mice showed a significant enhancement in mechanical allodynia up to 2 weeks post surgery (F (1, 24) = 43.61, P < 0.001). I) Neuropathic pain also produced a significant enhancement in the uninjected paw at 2 weeks.

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