Transient Receptor Potential Vanilloid: A Literature Review

Introduction
Pain occurs as a symptom as stimuli activate nociceptors because of an imbalance in the homeostasis of the tissue due to changes in the chemical, temperature and mechanical(12,15,17). This detection in the surrounding can be altered and therefore cause persistent pain in the body(1) and this sensitisation is therefore increased and modulated(8), such as in the visceral region. An example is Irritable Bowel Syndrome (IBS) which has chronic pain as a symptom. A receptor that has been seen to be present and upregulated in this disease are Transient Receptor Potential (TRP) channels, and in particular, Transient Receptor Potential Vanilloid type 1 (TRPV1) and Transient Receptor Potential Ankyrin Type 1 (TRPA1)(15,18). In this review, TRPV1 and other channels, such as TRPA1 induced pain are looked at. As possible drug targets, there have been studies with various antagonists, that have seen downregulation of expression of TRPV1, however, there are problematic side effects such as hyperthermia(3,17).

What are transient potential receptor channels?

TRP channels are polymodal(12) channels, so it is activated by various stimuli such as temperature, where the threshold
TRPV1 has a high affinity for Ca2+(3,5) which can be affected by inflammatory mediators, such as histamine which allows for more Ca2+ to enter the neuron, thus lowering the threshold(5,18). The TRP ion channel structure has “six transmembrane polypeptide subunits with a putative pore-loop region with a cytoplasmic amino terminus with three Ankyrin repeat domains and cytoplasmic carboxy-terminus” which are the characteristics of TRP channels(6). TRPA1, however, is a G-protein coupled receptor (GCPR), and when activated, like the other channels, will also increase its intracellular Ca2+(4,14). As the TRP channels are ion channels and GCPRs, they are targeted by analgesic