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. 2024 Jan;25(1):88–100. doi: 10.1016/j.jpain.2023.07.023

Figure 2.

Figure 2

Oxaliplatin alters the proportions of cold and mechanically sensitive A fibers profoundly. The number of fibers that respond to mechanical (black circles) or cold (blue circles) stimulation after vehicle (left-hand panel) or oxaliplatin treatment (right-hand panel) of the corresponding receptive field. Before incubation with vehicle or oxaliplatin, all fibers were identified using mechanical stimuli and were thus initially mechanosensitive. After vehicle treatment (20 minutes, glucose 5% in SIF), almost all AM (11/12), D-hair (4/6), AβRA (9/10) AβSA (10/10), CM (7/7), and CMC (10/10) fibers fired in response to mechanical step stimulation. Pre or postvehicle treatment, very few A fibers fired action potentials in response to a 60 seconds cold ramp to ∼5 to 8 °C (pretreatment control 2/22 AM-C, post-treatment 1/11). CMC fibers responded to cold ramp before and after vehicle treatment (10/10), CM fibers did not gain de novo cold responsiveness after vehicle treatment (0/10). In contrast, significant proportions of AM, D-hair and AβRA were no longer sensitive to mechanical stimuli (P < .05, Fisher’s exact test) after oxaliplatin treatment (20 minutes, 600 µM in SIF). Remarkably, AM, D-hair and AβRA fibers that retained mechanical sensitivity almost all displayed a novel aberrant cold responsiveness. After oxaliplatin treatment, AβSA, CM, and CMC fibers retained mechanical sensitivity, but a subset of AβSA and CM fibers gained a novel cold sensitivity. *P < .05, **P < .01, ***P < .001, compared to vehicle, Fisher’s exact test. †P < .05, ††P <.01, †††P < .001, compared to pretreatment, Fisher’s exact test. Abbreviation: AβSA, Aβ slowly adapting fiber.