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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Coexistence of chronic hyperalgesia and multilevel neuroinflammatory responses after experimental SCI: a systematic approach to profiling neuropathic pain

Fig. 2

The data of sensorimotor behavioral evaluations of neurological reflexes, mechanical hypersensitivity, and bilateral or unilateral thermal hypersensitivity. A–E Spinal neurological reflexes. At day 1 post-injury (p.i.), SCI rats showed severe loss of contact righting reflex (A), proprioceptive positioning reflex of paw placing (B), and withdrawal reflex in response to brief extension of joints (C), which recovered overtime, with 80% SCI rats performing normally by 3 (A, C) or 4 weeks p.i. (B). Withdrawal reflexes caused by pressuring (D) and brief pinching (E) of the hindpaw exhibited discernible abnormalities p.i., with their recovery rates noticeably slower and more incomplete, relative to that of the righting (A), placing (B), or extension (C) reflex. By 8 weeks p.i., only ~ 33% SCI rats showed a normal nociception reflex (E). F–H Results of the modified von Frey filament tests of mechanical hypersensitivity (mVFT; F). In contrast to a stable array of sensitivity thresholds of the control group, at day 1 p.i., the mean threshold to trigger a withdrawal response following mVF stimulation drastically increased in the forepaws (G; 11.1 ± 1.5 g) and hindpaws (H; 45.8 ± 5.1 g) in the SCI rats. Afterward, the group mean threshold, compared to the pre-SCI level and control group, significantly decreased in the forepaws (i.e., above-injury level allodynia; G) and hindpaws (i.e., below-injury level allodynia; H), starting in 2 weeks after SCI. At-injury level allodynia measured in the dorsal dermatomes adjacent to the T10 injury had a comparable pattern of hypersensitivity (I; *p < 0.01 to < 0.001; n = 12/SCI or 10/control; two-way repeated measures ANOVA with Sidak’s post hoc test). J, K Data of bilateral and unilateral hot plate tests (i.e., thermal hypersensitivity/allodynia). In the bilateral hot plate test, the pre-SCI and pre-laminectomy mean hindlimb latencies were statistically indistinguishable and the control group showed steady postsurgical response latencies (J). At day 1 p.i., the group mean latency markedly increased (19.1 ± 3.1 s) in the injured rats. Starting in week 3 after SCI, thermal hypersensitivity developed, which remained continuous and significantly different than the baseline values and those of the control group (J; SCI: n = 12, laminectomy: n = 10; *p < 0.05–0.001; two-way repeated measures ANOVA with Sidak’s post hoc test). The unilateral hindlimb hot plate test revealed a similar pattern of response latency changes. However, this test detected significantly reduced group mean latencies 1 week earlier, starting on day 14 p.i., compared to the baseline level and control group (K; n = 12/SCI or 10/control; *p < 0.05 to < 0.001; two-way repeated measures ANOVA with Sidak’s post hoc test; note: to make the figure succinct, the gentle body holding logistics were not depicted in the inset)

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