Forty years in capsaicin research for sensory pharmacology and physiology

Szolcsányi, Janós

doi:10.1016/j.npep.2004.07.005

Cited by 318 publications

(223 citation statements)

References 19 publications

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“…2C). These data were in a marked contrast to those seen on sensory neurons and on most of the TRPV1-expressing non-neuronal cells where capsaicin induced a massive, mostly Ca 2+ -dependent cytotoxicity [1][2][3]17,19]. Apparently, the Ca 2+ -handling S1).…”

Section: Trpv1-signaling Inhibits DC Differentiationmentioning

confidence: 89%

Transient receptor potential vanilloid‐1 signaling inhibits differentiation and activation of human dendritic cells

et al. 2009

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a b s t r a c tThe goal of the current study was to investigate the expression of transient receptor potential vanilloid-1 (TRPV1) on human in vitro differentiated monocyte-derived dendritic cells (DCs) and to dissect the corresponding role of TRPV1-signaling in DC-specific functions. TRPV1 expression was identified both at the protein and gene levels in human DCs. Moreover, the prototypic TRPV1 agonist capsaicin specifically (i.e. via TRPV1) and dose-dependently inhibited cytokine-induced DC differentiation, phagocytosis of bacteria, activation of DCs, and pro-inflammatory cytokine secretion. These data introduce TRPV1-coupled signaling as a novel player in human monocyte-derived DC biology with anti-inflammatory actions.

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Section: Trpv1-signaling Inhibits DC Differentiationmentioning

confidence: 89%

Transient receptor potential vanilloid‐1 signaling inhibits differentiation and activation of human dendritic cells

et al. 2009

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“…The heat-sensitive channel TRPV3, a potential warm receptor with a threshold of 31°-39°C (Smith et al 2002;Xu et al 2002;Peier et al 2002b), has been reported to be co-expressed in DRG neurons (Smith et al 2002) with the capsaicin and heat-sensitive channel TRPV1 (Caterina et al 1999;Szolcsanyi 2004). In addition, TRPV3 continues to respond to painfully hot temperatures (Peier et al 2002b) knockout mice that lack TRPV3 show deficits in response to both noxious and innocuous heat (Moqrich et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Nociceptive sensations evoked from ‘spots’ in the skin by mild cooling and heating

Green

Roman

Schoen

et al. 2008

Pain

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It was recently found that nociceptive sensations (stinging, pricking, or burning) can be evoked by cooling or heating the skin to innocuous temperatures (e.g., 29°, 37°C). Here we show that this lowthreshold thermal nociception (LTN) can be traced to sensitive 'spots' in the skin equivalent to classically defined warm spots and cold spots. Because earlier work had shown that LTN is inhibited by simply touching a thermode to the skin, a spatial search procedure was devised that minimized tactile stimulation by sliding small thermodes (16 mm 2 and 1 mm 2 ) set to 28° or 36°C slowly across the lubricated skin of the forearm. The procedure uncovered three types of temperature-sensitive sites (thermal, bimodal and nociceptive) that contained one or more thermal, nociceptive or (rarely) bimodal spots. Repeated testing indicated that bimodal and nociceptive sites were less stable over time than thermal sites, and that mechanical contact differentially inhibited nociceptive sensations. Intensity ratings collected over a range of temperatures showed that LTN increased monotonically on heat-sensitive sites but not on cold-sensitive sites. These results provide psychophysical evidence that stimulation from primary afferent fibers with thresholds in the range of warm fibers and cold fibers is relayed to the pain pathway. However, the labile nature of LTN implies that these lowthreshold nociceptive inputs are subject to inhibitory controls. The implications of these findings for the roles of putative temperature receptors and nociceptors in innocuous thermoreception and thermal pain are discussed.

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“…The action of capsaicin is mediated by capsaicin receptor which was cloned and named as transient receptor potential vanilloid-1 (TRVP1) [75], the specific sensor for capsaicin [76][77][78][79].…”

Section: Capsaicin-sensitive Primary Afferent Neurons and Transient Rmentioning

confidence: 99%

The Role of Capsaicin-Sensitive Afferent Nerves in Gastric Mucosal Protection Initiated Centrally or Peripherally under Experimental Conditions

Gyires¹

2014

Capsaicin - Sensitive Neural Afferentation and the Gastrointestinal Tract: From Bench to Bedside

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Forty years in capsaicin research for sensory pharmacology and physiology

Cited by 318 publications

References 19 publications

Transient receptor potential vanilloid‐1 signaling inhibits differentiation and activation of human dendritic cells

Transient receptor potential vanilloid‐1 signaling inhibits differentiation and activation of human dendritic cells

Nociceptive sensations evoked from ‘spots’ in the skin by mild cooling and heating

The Role of Capsaicin-Sensitive Afferent Nerves in Gastric Mucosal Protection Initiated Centrally or Peripherally under Experimental Conditions

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