The neurobiology of itch

@article{Ikoma2006TheNO,
  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},
  year={2006},
  volume={7},
  pages={535-547}
}
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
TLDR
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
TLDR
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
TLDR
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
TLDR
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].
TLDR
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.
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References

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TLDR
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.
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TLDR
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TLDR
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TLDR
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Itching for an explanation
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TLDR
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
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  • Biology
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TLDR
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.
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TLDR
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).
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