The neurobiology of itch

  title={The neurobiology of itch},
  author={Akihiko Ikoma and Martin Steinhoff and Sonja St{\"a}nder and Gil Yosipovitch and Martin Schmelz},
  journal={Nature Reviews Neuroscience},
The neurobiology of itch, which is formally known as pruritus, and its interaction with pain have been illustrated by the complexity of specific mediators, itch-related neuronal pathways and the central processing of itch. Scratch-induced pain can abolish itch, and analgesic opioids can generate itch, which indicates an antagonistic interaction. However, recent data suggest that there is a broad overlap between pain- and itch-related peripheral mediators and/or receptors, and there are… 
Anatomy and neurophysiology of pruritus.
Updated neurophysiology of itch.
  • A. Ikoma
  • Biology
    Biological & pharmaceutical bulletin
  • 2013
The unique physiological features of histamine-sensitive C-fibers and spinothalamic tract neurons support the hypothesis of itch specific pathway, whereas subsequent studies on cowhage-induced itch
Histamine-induced itch and its relationship with pain
The molecular mechanism and the pharmacological aspects of histamine-induced itch are discussed and it appears that itch and pain involve different neuronal pathways.
Recent Advances in the Study of Itching
The unique physiological features of histamine-sensitive C-fibers and spinothalamic tract neurons support the hypothesis of itch specific pathway, whereas subsequent studies on cowhage-induced itch
Neurophysiology of Itch
The finding that histamine-induced itch is conducted by mechano-insensitive nerves has suggested the presence of itch-specific neuronal pathways, which can originate from neuronal disorders as well as systemic diseases.
The peripheral and central mechanisms underlying itch
This review summarizes recent progress in the study of itch, focusing on itch-selective receptors, signaling molecules, neuronal pathways from the primary sensory neurons to the brain, and potential decoding mechanisms based on which itch is distinguished from pain.
Modulation of Pruritus: Peripheral and Central Sensitisation
It appears obvious to use a common research strategy to better understand the mechanism leading to chronic pain and chronic itch.
[Opioid-induced pruritus. Mechanisms and treatment regimens].
It is now clear that opioids can also induce itching at the spinal level and activation of mu-opioid receptors (mu-OR), while kappa-OR surprisingly suppress itch.


Neurophysiological, neuroimmunological, and neuroendocrine basis of pruritus.
This review summarizes the current information about the significance of neuron-skin interactions, ion channels, neuropeptides, proteases, cannabinoids, opioids, kinins, cytokines, biogenic amines, neurotransmitters, and their receptors in the pathobiology of pruritus.
Relief of intractable pruritus with naloxone.
The central itch-provoking effect of morphine is intriguing in light of recent evidence of the existence of central opiate receptors and naturally occurring peptides with opiate activity in the mammalian body.
Neurophysiology of pruritus: cutaneous elicitation of itch.
Investigations have revealed new receptor systems on cutaneous sensory nerve fibers that may modulate itch and thereby represent targets for antipruritic therapy, including neurotransmitters, neuropeptides, and inflammatory mediators.
Frontiers in pruritus research: scratching the brain for more effective itch therapy.
This Review highlights selected frontiers in pruritus research and focuses on recently attained insights into the neurophysiological, neuroimmunological, and neuroendocrine mechanisms underlying
Brain activation by histamine prick test-induced itch.
Itch is a well-known dermatological symptom whose reactions in the brain have been studied very less, and brain responses to longer-lasting histamine reaction in healthy participants were tested.
Itching for an explanation
Histamine-induced itch converts into pain in neuropathic hyperalgesia
Physiologically, itch and pain are transmitted in separate specific peripheral C-units and central afferent pathways and in neuropathies irritable nociceptors may express histamine receptors or induce central sensitization to histaminergic stimuli so that itch converts into pain.
ET – phone the pain clinic
  • G. Nicol
  • Biology
    Trends in Neurosciences
  • 2004
Effects of classical algogens
Recruitment of unmyelinated afferents and sustained non-adapting activity occur when moderately low pH and inflammatory mediators combine to mimick the inflammatory exclude, which maintains a primary afferent input from inflamed tissue to the central nervous system.
Itch: scratching more than the surface.
Drug treatments for itch include rifampicin, colestyramine and 17-alpha alkyl androgens (cholestasis), thalidomide (uraemia), cimetidine and corticosteroids (Hodgkin's lymphoma), paroxetine (paraneoplastic itch), aspirin and paroxETine (polycythaemia vera) and indometacin (some HIV+ patients).