A functional unbalance of TRPM8 and Kv1 channels underlies orofacial cold allodynia induced by peripheral nerve damage.

ABSTRACT: Cold allodynia is a debilitating symptom of orofacial neuropathic pain resulting from trigeminal nerve damage. The molecular and neural bases of this sensory alteration are still poorly understood. Here, using chronic constriction injury (CCI) of the infraorbital nerve (IoN) (IoN-CCI) in mice, combined with behavioral analysis, Ca²⁺ imaging and patch-clamp recordings of retrogradely labeled IoN neurons in culture, immunohistochemistry, and adeno-associated viral (AAV) vector-based delivery in vivo, we explored the mechanisms underlying the altered orofacial cold sensitivity resulting from axonal damage in this trigeminal branch. We found that cold allodynia induced by IoN-CCI is linked to an increase in the proportion of cold-sensitive neurons (CSNs) contributing to this

SUBMITTER: Pina R 

PROVIDER: S-EPMC11655194 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature