Itch-associated response induced by intradermal serotonin through 5-HT2 receptors in mice

  title={Itch-associated response induced by intradermal serotonin through 5-HT2 receptors in mice},
  author={Tomomi Yamaguchi and Tetsuro Nagasawa and Masamichi Satoh and Yasushi Kuraishi},
  journal={Neuroscience Research},

Attenuation of serotonin-induced itch by sumatriptan: possible involvement of endogenous opioids

It is shown that intradermal and intraperitoneal administration of sumatriptan significantly reduce 5-HT-induced scratching behavior in mice, and combined treatment with sub-effective doses of sum atriptan and an opioid receptor antagonist, naltrexone, decreases 5- HT-evoked scratching responses.

5‐HT3 receptors antagonists reduce serotonin‐induced scratching in mice

It is shown that the scratching induced by intradermal serotonin is mediated by 5‐HT3 receptors subtype, which means that 5-HT3 may play a role in mediating serotonin‐associated itch responses, and 5‐ HT3 receptors as possible targets for antipruritic agents are introduced.

5-Hydroxytryptamine (5-HT)2 Receptor Involvement in Acute 5-HT-Evoked Scratching but Not in Allergic Pruritus Induced by Dinitrofluorobenzene in Rats

Intradermal injection of α-methylserotonin, a 5-HT2 receptor agonist, elicited scratching behavior in a dose-dependent manner, indicating that acute5-HT-induced scratching is mediated via peripheral 5- HT2 receptors.

Intradermal nociceptin elicits itch-associated responses through leukotriene B(4) in mice.

The results suggest that nociceptin acts on ORL1 receptor on the keratinocytes to produce leukotriene B(4), which induces itch-associated responses in mice.

Intracisternal, but not intrathecal, injection of naloxone inhibits cutaneous itch-related response in mice.

It is suggested that mu-opioid receptor in the lower brainstem, but not spinal cord, is a site of central pruritogenic action of opioids and is involved in the facilitatory regulation of itch signaling.

Pharmacological characterization of itch-associated response induced by repeated application of oxazolone in mice.

Results suggest that leukotriene B(4) receptor and M(3) muscarinic acetylcholine receptor are involved in the itch-associated response induced by repeated application of oxazolone in mice.

Serotonin Receptor 2B Mediates Mechanical Hyperalgesia by Regulating Transient Receptor Potential Vanilloid 1

5-HT2B mediates 5-HT-induced mechanical hyperalgesia by regulating TRPV1 function through the Gq/11-phospholipase Cβ-protein kinase Cε pathway mediated by 5- HT2B.

Intradermal cholinergic agonists induce itch-associated response via M3 muscarinic acetylcholine receptors in mice.

Muscarinic agonists are suggested to produce itch through activation of M3 muscarinic receptors in the skin throughactivation of M2 muscaric receptors inThe skin.



Substance P induction of itch-associated response mediated by cutaneous NK1 tachykinin receptors in mice.

The results suggest that scratching of the mouse induced by an i.d. injection of SP is itch-associated response, and the SP action may be mediated at least partly by cutaneous NK1 receptors, and mast cells may not be key factors in SP-induced itching.

Can a serotonin type 3 (5-HT3) receptor antagonist reduce experimentally-induced itch?

Serotonin has an own pruritic potency and does not only act over histamine containing mast cells and could significantly reduce serotonin-induced flares after pretreatment with an orally applied antihistamine.

Intracisternal injection of opioids induces itch-associated response through mu-opioid receptors in mice.

It is suggested that morphine and DAMGO increased facial scratching, probably mediated by central opioid mu-receptors in mice, and such scratching was due to a sensation, probably itching.

Scratching behavior induced by pruritogenic but not algesiogenic agents in mice.


The enhancing effect of naloxone may be due to an antagonism of endogenous ligands for the opiate receptor and these ligands would be involved in reaction to but not in perception of nociceptive stimuli which need not be harmful ones.