Pain transduction: a pharmacologic perspective

Abstract

Pain represents a necessary physiological function yet remains a significant pathological process in humans across the world. The transduction of a nociceptive stimulus refers to the processes that turn a noxious stimulus into a transmissible neurological signal. This involves a number of ion channels that facilitate the conversion of nociceptive stimulus into an electrical signal. Because an understanding of nociceptive physiology complements a discussion of analgesic pharmacology, the relationships between the two are presented together. In this review article, a critical evaluation is provided on the findings relating to both the physiology and pharmacology of relevant acid-sensing ion channels (ASIC), and transient receptor potential (TRP) cation channels, and voltage-gated sodium (Nav) channels.

Menthol, a unique urinary volatile compound, is associated with chronic inflammation in interstitial cystitis

“…joint aches), noxious heat, sensory hypersensitivity, sore throat et al . The analgesic and anti-inflammatory effects of menthol may be attributed to the fact that it is a TRPM8 agonist 29 , 30 . However, the underlying mechanisms of menthol’s biological effects remain obscure.…”

Topical Phenytoin in Neuralgic Pain, Peripheral Modulation of Central Sensitization: Two Case Reports

“…Anesthetics that block such channels need therefore to be administered topically or locally to avoid undesired, systemic side effects, such as with IV lidocaine. Sodium channels however, are also to be found in the skin, and especially on the keratinocytes [28]. It is here, that the inhibitory feedback from the periphery to the central nervous system, as hypothesized by Baron and Dickenson starts.…”

“…Nav 1.3, 1.7, 1.8, and 1.9 most probably are channels for nociceptive transduction. Sadly enough only fragmentary insight exists in the role and the peripheral expression of sodium channels in pain-transducing free nerve ending in the skin and on the keratinocytes [28]. The sodium channels, Nav1.1, Nav1.6 and Nav1.8 are abundantly present at epidermal keratinocytes [29].…”

Hypervigilance in the Detection of Early Complex Regional Pain Syndrome, Type 1/Reflex Sympathetic Dystrophy—An Underutilized Tool in Treatment

“…Pain perception is the consequence of several steps in the processing of 'pain' signals from peripheral receptors through perception of pain at the cortex. [44][45][46] These processes include signal transduction, transmission, modulation, and perception. Additionally, excitatory molecules and inflammatory mediators contribute to the phenomena that alter the orderly process of signal processing through peripheral sensitization, wind-up, and central sensitization.…”