In a recent study published in Scientific Reports, the team of Aziz Moqrich used a combination of mouse genetics and behavioral pharmacology to unravel the functional specialization of GINIP-expressing neurons. These neurons encompass two subsets of anatomically and functionally distinct populations of neurons: the free nerve ending cutaneous MRGRPD+ neurons; specialized in sensing noxious mechanical stimuli and the C-Low Threshold MechanoReceptors (C-LTMRs); whose function was unknown. They showed that genetic ablation of GINIP-expressing neurons in a living mouse led to a significant decrease of formalin-evoked first pain response and a nearly complete loss of the second pain response. Knowing that MRGRPD+ neurons are dispensable for formalin-evoked pain, their study strongly suggests that C-LTMRs are likely required to convey the prototypical biphasic pain response mediated by formalin. This study also confirmed a previous work of Delfini and Mantilleri et al., Cell Reports 2013) in which the team indirectly postulated the role of this particular subset of sensory neurons in modulating formalin-evoked pain.

Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain.
Urien L, Gaillard S, Lo Re L, Malapert P, Bohic M, Reynders A, Moqrich A.
Sci Rep. 2017 Feb 27;7:43493. doi: 10.1038/srep43493.

Aziz Moqrich (