The Cells and Circuitry for Itch Responses in Mice

Itch is triggered by somatosensory neurons expressing the ion channel TRPV1 (transient receptor potential cation channel subfamily V member 1), but the mechanisms underlying this nociceptive response remain poorly understood. Here, we show that the neuropeptide natriuretic polypeptide b (Nppb) is ex...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2013-05, Vol.340 (6135), p.968-971
Main Authors: Mishra, Santosh K., Hoon, Mark A.
Format: Article
Language:English
Subjects:
Animals
Chloroquine - pharmacology
Endothelin-1 - pharmacology
gastrin-releasing peptide
Gastrin-Releasing Peptide - metabolism
Gastrin-Releasing Peptide - pharmacology
Glass fiber reinforced plastics
Histamine - pharmacology
Histamines
Horns
Interneurons
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Natriuretic Peptide, Brain - genetics
Natriuretic Peptide, Brain - metabolism
Natriuretic Peptide, Brain - pharmacology
nerve fibers
Neurology
Neurons
Neuropeptides
Neuroscience
Neurotransmitters
Nociception
Peptides
Phospholipase C beta
Polypeptides
Pruritus - chemically induced
Pruritus - metabolism
Pruritus - physiopathology
Receptors
Receptors, Atrial Natriuretic Factor - metabolism
Rodents
Sensory neurons
Sensory Receptor Cells - drug effects
Sensory Receptor Cells - metabolism
Signals
Spinal cord
Spinal Cord - drug effects
Spinal Cord - pathology
Spinal Cord - physiopathology
Switches
TRPV Cation Channels - metabolism
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Summary:Itch is triggered by somatosensory neurons expressing the ion channel TRPV1 (transient receptor potential cation channel subfamily V member 1), but the mechanisms underlying this nociceptive response remain poorly understood. Here, we show that the neuropeptide natriuretic polypeptide b (Nppb) is expressed in a subset of TRPV1 neurons and found that Nppb -/- mice selectively lose almost all behavioral responses to itch-inducing agents. Nppb triggered potent scratching when injected intrathecally in wild-type and Nppb -/- mice, showing that this neuropeptide evokes itch when released from somatosensory neurons. Itch responses were blocked by toxin-mediated ablation of Nppb-receptor-expressing cells, but a second neuropeptide, gastrin-releasing peptide, still induced strong responses in the toxin-treated animals. Thus, our results define the primary pruriceptive neurons, characterize Nppb as an itch-selective neuropeptide, and reveal the next two stages of this dedicated neuronal pathway.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.1233765