Potentiation and suppression of the histamine response by raising and lowering the temperature in canine visceral polymodal receptors in vitro

Mizumura, Kazue; Koda, Hisashi

doi:10.1016/s0304-3940(99)00257-8

Cited by 25 publications

(13 citation statements)

References 8 publications

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“…It is commonly experienced as well as tested experimentally that warming aggravates itch (Mizumura and Koda, 1999), whereas itch is suppressed by noxious heat. The most probable explanation for aggravation of itch by warming would be that TRPV1 is sensitized by inflammatory factors in pathological condition in skin such as dermatitis, which possibly lowers the heat threshold (Sugiura et al, 2002;Moriyama et al, 2005) and increases the sensitivity to endogenous ligands in TRPV1 activation.…”

Section: Discussionmentioning

confidence: 99%

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A₂and 12-Lipoxygenase

Shim¹,

Tak²,

Lee³

et al. 2007

J. Neurosci.

409

382

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Histamine provokes itching and is a major skin disease complaint. Histamine is known to excite a subset of sensory neurons, predominantly C-fibers. Although histamine is pruritogenic, its signaling pathways that excite sensory neurons have not been identified. Because the metabolic products of lipoxygenases (LOs) activate transient receptor potential vanilloid receptor-1 (TRPV1) in sensory neurons, we hypothesized that histamine excites sensory neurons by activating TRPV1 via phospholipase A 2 (PLA 2 ) and LO stimulation. In cultured sensory neurons, histamine evoked inward currents that were reduced by capsazepine, a TRPV1 blocker. Moreover, histamine provoked inward currents when histamine receptor subtype 1 (H1R) and TRPV1 were expressed heterologously, but not when H1R or TRPV1 was expressed alone. In addition, histamine caused Ca 2ϩ influxes in sensory neurons in wild-type mice but not in TRPV1 Ϫ/Ϫ mice. Furthermore, histamine caused a 2.5-fold increase in the production of 12-hydroxyeicosatetraenoic acid, a metabolite of LO, in cultured sensory neurons. When injected subcutaneously into the necks of mice, histamine caused bouts of scratching, which were greatly reduced by pretreatment with capsazepine, a TRPV1 blocker, and by inhibitors of PLA 2 , LO, and H1R. Furthermore, mice lacking TRPV1 markedly reduced histamine-induced scratching compared with wild type. Together, these results indicate that TRPV1 plays a key role in mediating the pruritogenic action of histamine via the PLA 2 /LO pathway.

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Section: Discussionmentioning

confidence: 99%

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A₂and 12-Lipoxygenase

Shim¹,

Tak²,

Lee³

et al. 2007

J. Neurosci.

409

382

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show abstract

“…Other groups of mediators and receptors play a role in both pain and pruritus suppression peripherally and/or centrally and thereby represent targets of antinociceptive therapy ( Table 1). They mediate non-painful sensations such as cold and relief of itch and pain (Mizumura and Koda, 1999). In the central nervous system, l-opioid receptors suppress pain, but induce pruritus while j-opioid receptors relief pruritus.…”

Section: Suppression Of Histamineinduced Itchmentioning

confidence: 99%

Chronic itch and pain—Similarities and differences

Ständer

Schmelz

2006

European Journal of Pain

142

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Both, pruritus and pain are aversive, but clearly distinct sensations originating in the peripheral and central nervous system. During the last years, many interactions between itch and pain in acute transmission and sensitization processes have been identified. It is common experience that the itch sensation can be reduced by the painful sensations caused by scratching. Vice versa analgesia may reduce this inhibition and thus enhance itch. This phenomenon is particularly relevant to spinally administered mu-opioid receptor agonists, which induce segmental analgesia often combined with segmental pruritus. The peripheral and central sensitization to pain and to itch exhibits striking similarities. Classical inflammatory mediators such as bradykinin have been shown to sensitize nociceptors for both itch and pain. Also regulation of gene expression induced by trophic factors, such as NGF, plays a major role in persistently increased neuronal sensitivity for itch and pain. Finally, itch and pain exhibit corresponding patterns of central sensitization. The knowledge of antagonistic interaction, but also of similar sensitization processes has major implication for antipruritic therapeutic approaches.

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“…Central inhibition of itch can also be achieved by cold stimulation. In addition, cooling has a peripheral inhibitory effect: histamine‐induced activation of nociceptors can be reduced by cooling (12). Also, in humans cooling of a histamine‐treated skin site reduced the activity of the primary afferents and decreased the area of “itchy skin” or “hyperknesis” around the application site (13) (see following discussion).…”

Section: Inhibition Of Pain May Enhance Pruritusmentioning

confidence: 99%

Itch and pain

Schmelz

2005

Dermatologic Therapy

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The discovery of a specialized neuronal pathway for itch has markedly improved our understanding of itch processing under physiological conditions. However, the complex interactions of pain and itch are only partly understood. This review focuses on the neurophysiological mechanisms involved in clinical and experimental itch conditions. There is emerging evidence that similar patterns of peripheral and central sensitization occur in chronic pain and chronic itch conditions. It will be of major interest to reveal whether the underlying mechanism for sensitization in the itch and pain pathways are also similar, as this might have major implications for therapy.

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Potentiation and suppression of the histamine response by raising and lowering the temperature in canine visceral polymodal receptors in vitro

Cited by 25 publications

References 8 publications

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A₂and 12-Lipoxygenase

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A₂and 12-Lipoxygenase

Chronic itch and pain—Similarities and differences

Itch and pain

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Potentiation and suppression of the histamine response by raising and lowering the temperature in canine visceral polymodal receptors in vitro

Cited by 25 publications

References 8 publications

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A2and 12-Lipoxygenase

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A2and 12-Lipoxygenase

Chronic itch and pain—Similarities and differences

Itch and pain

Contact Info

Product

Resources

About

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A₂and 12-Lipoxygenase

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A₂and 12-Lipoxygenase