Morphological Correlates of TRPV1 Agonist-Induced Activation and Defunctionalization of Nociceptor Neurons.

Transient receptor potential vanilloid type 1 (TRPV1) agonist-induced analgesia is a current hot topic of pain research and a promising possibility to alleviate chronic/neuropathic pain. Local applications in humans and animals and systemic administration in experimental animals of TRPV1 agonists have been demonstrated to produce a long-lasting blockade of nociceptors leaving the function of other types of sensory nerves, as well as autonomic and motor nerve fibers, intact. Morphological studies revealed that TRPV1 agonist-mediated drug action is linked to distinct structural alterations involving reversible and/or irreversible neuronal degenerative processes. This review is intended to summarize the available information on morphological changes associated with TRPV1 agonist-induced activation and defunctionalization of nociceptors expressing the TRPV1/capsaicin receptor. In addition, morphological alterations associated with some pathologies involving TRPV1-expressing nociceptors will also be dealt with. Activation and defunctionalization can be elicited from any domain of TRPV1 receptor-expressing neurons. Considering the similar membrane properties of perikarya, axons and peripheral receptive nerve endings, the term chemosensitive nociceptor neuron is proposed to denote this particular class of primary sensory neurons.