Nociceptin/orphanin FQ (N/OFQ) acts through the N/OFQ peptide receptor (NOP) [ 3] and can change responsiveness to painful stimuli in several models of pain [ 4– 6].
In animal models of pain, RTX has also been found useful in inflammatory pain, painful conditions affecting joints, and bone cancer pain by eliminating TRPV1 expressing peripheral nerve terminals or DRG neurons [21], [22], [23], [24].
However, electrophysiological studies in animal models of pain are limited.
URB937, a FAAH inhibitor specific to peripheral tissues, causes analgesia in animal models of pain [1].
Experimental studies in human models of pain suggest that nicotine has analgesic properties [21, 22].
Despite its limited distribution, URB937 exhibits marked analgesic properties in rodent models of pain.
Our findings strongly encourage the study of ANA in models of pain in general and of migraine in particular.
Animal models of pain are designed to mimic distinct clinical diseases to better evaluate underlying mechanisms and potential treatments.
There are experimental results suggesting the role of PACAP in the development of peripheral sensitization as well in certain models of pain [78].
Interestingly, CB2 agonists can reduce nociception in several preclinical models of pain without producing tolerance [9] or central side-effects [11].
Thus, findings produced by using selective thermo-TRP antagonists may better unveil the role of these channels in models of pain diseases.
