Nociception in a Progressive Multiple Sclerosis Model in Mice Is Dependent on Spinal TRPA1 Channel Activation

Periorbital Nociception in a Progressive Multiple Sclerosis Mouse Model Is Dependent on TRPA1 Channel Activation

“…MOG 35–55 and CFA administration elicited an increase in clinical scores that started at day 13 p.i. ( Figure S1A, Supplementary Materials ), indicating the onset of PMS-EAE, as previously reported [ 44 ]. Nevertheless, no changes in locomotor activity ( Figure S1B, Supplementary Materials ) or body weight ( Figure S1C, Supplementary Materials ) between the PMS-EAE and the control groups were detected during the 14 days of observation.…”

“…Nevertheless, no changes in locomotor activity ( Figure S1B, Supplementary Materials ) or body weight ( Figure S1C, Supplementary Materials ) between the PMS-EAE and the control groups were detected during the 14 days of observation. However, as the animals after 14 days showed motor impairment and weight loss, we selected this time point to perform our study, as our previous publication that used this PMA-EAE model [ 44 ]. In addition, the periorbital mechanical threshold of PMS-EAE mice was 0.0126 ± 0.0002 g; for control it was 0.4273 ± 0.2177 g 14 days p.i., which shows that the PMS-EAE-induced mice had a very low threshold considering that the lowest von Frey filament used was 0.008 g.…”

“…Previously, we showed the development of neuropathic pain-like behaviours, without motor impairment, with a nociception peak 14 days p.i. of PMS-EAE for mechanical and cold allodynia assessed in the hind paw [ 44 ]. We have not evaluated the PMA after 14 days p.i.…”

“…HC-030031 and A-967079, when administered in mice in the doses used in this study, show antinociceptive effects for 1–2 h in other pain models [ 9 , 67 ]. Additionally, these TRPA1 antagonists (HC-030031, A-967079, metamizole, and propyphenazone) have antinociceptive effects during the mechanical and cold allodynia measurement in a neuropathic pain behaviour induced by PMS-EAE after 1–2 h [ 44 ].…”

“…Previously, our group described the relation between the development of neuropathic pain-like behaviours and TRPA1 activation induced by two different MS mouse models: the PMS-EAE and the relapsing-remitting multiple sclerosis (RR-EAE) models [ 43 , 44 ]. Thus, our main purpose was to optimise the development of PMA in a PMS-EAE model and detect the role of TRPA1 in this nociceptive behaviour.…”