**5. Conclusions**

Antagonism of the TRPA1 channel by means of ADM\_12 attenuates experimentally-induced mechanical allodynia [17,119] in a reliable animal model of trigeminal neuropathic pain. Allodynia is one of the major clinical features of trigeminal neuropathic pain [120,121], thus the modulation of the TRPA1 channel may represent a suitable therapeutic target [122,123], and ADM\_12 a possible tool, in trigeminal neuropathic pain management. As a corollary, our data also suggests a possible role for TRPV1 channels in the behavioral and biomolecular responses related to trigeminal neuropathic pain. Further exploration of the mechanisms underlying the antinociceptive effects of TRPA1, and studies directed to better understand the relationship between TRPA1 and TRPV1, would improve our understanding of the complex nociceptive processing in trigeminal neuropathic pain.

**Author Contributions:** C.D.: Conceptualization, Investigation, Formal analysis, Writing—original draft; R.G.: Conceptualization, Writing—review & editing; A.M.Z.: Investigation; O.F.: Methodology; C.N.: Writing—review & editing; C.T.: Funding acquisition, Writing—review & editing; K.D.: Conceptualization, Supervision, Investigation, Writing—review & editing. All authors read and approved the final manuscript.

**Funding:** This research was funded by a grant of the Italian Ministry of Health (Ricerca Corrente, 2016) to the IRCCS Mondino Foundation.

**Acknowledgments:** The authors would like to thank Stefania Ceruti for her precious suggestions during the writing of the manuscript.

**Conflicts of Interest:** The authors declare no conflict of interest.
