Outcomes caused by the interactions between sensory TRPs and lipid ligands are also discussed. Isoprene lipids, diacylglycerol, resolvin, and lysophospholipids also show distinct activities on sensory TRP channels. Unsaturated fatty acids or their metabolites via lipoxygenase, cyclooxygenase or epoxygenase are able to modulate (activate, inhibit or potentiate) the function of specific TRPs. Here, we focus on endogenously generated lipids that modulate the sensory TRP activities. Evidence is growing that lipidergic substances are also cable of modifying TRP ion channel activity by direct binding. Natural and synthetic compounds have been found to act on these sensory TRP channels to alter the nociception. Cation influx through activated TRP ion channels depolarizes the plasma membrane, resulting in neuronal excitation and pain. Six transient receptor potential (TRP) ion channels are expressed in the sensory nerve terminals and play a crucial role in sensing diverse noxious stimuli. The sensory nerves relay these signals by electrical discharges to the brain, leading to pain perception.
Environmental or internal noxious stimuli excite the primary sensory nerves in our body.
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