A recent study, using laboratory mice, discovered a physical link within the brain that may explain why headaches are more severe than pain we experience in other parts of the body. Pain perception involves both the physical sensation of pain and the emotional response to that pain. There are physical structures within the brain that regulate both, but until now, a direct link between the two had only been hypothesized.
An ability to adapt to changes in oxygen availability is essential for survival in both prokaryotic and eukaryotic organisms. Recently, cation channels encoded by the transient receptor potential (trp) gene superfamily have been recognized as multimodal sensors of a wide variety of factors inside the cells and in the extracellular environment and also as transducers of electrical and chemical signals mediated by ions such as Ca2+.
Transient receptor potential (TRP) channels, a family of structurally related proteins have been implicated in the sensation of pain and hyperalgesia caused by exogenous and endogenous agonists, as well as touch, pH, and temperature. The objective of this study was to determine the effects of tooth injury on the expression of the cold sensitive channel TRPA1, in the trigeminal ganglion, the primary source of sensory and nociceptive innervation of teeth.
The California bay laurel or Umbellularia californica (Hook. & Arn.) Nutt., is known as the ‘headache tree’ because the inhalation of its vapours can cause severe headache crises. However, the underlying mechanism of the headache precipitating properties of Umbellularia californica is unknown. The monoterpene ketone umbellulone, the major volatile constituent of the leaves of Umbellularia californica, has irritating properties, and is a reactive molecule that rapidly binds thiols.
Pain perception begins with the activation of primary sensory nociceptors. Over the past decade, flourishing research has revealed that members of the Transient Receptor Potential (TRP) ion channel family are fundamental molecules that detect noxious stimuli and transduce a diverse range of physical and chemical energy into action potentials in somatosensory nociceptors. Here we highlight the roles of TRP vanilloid 1 (TRPV1), TRP melastatin 8 (TRPM8) and TRP ankyrin 1 (TRPA1) in the activation of nociceptors by heat and cold environmental stimuli, mechanical force, and by chemicals including exogenous plant and environmental compounds as well as endogenous inflammatory molecules.