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      The cells and circuitry for itch responses in mice.

      Science (New York, N.Y.)

      Animals, Chloroquine, pharmacology, Endothelin-1, Gastrin-Releasing Peptide, metabolism, Histamine, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Natriuretic Peptide, Brain, genetics, Nociception, Phospholipase C beta, Pruritus, chemically induced, physiopathology, Receptors, Atrial Natriuretic Factor, Sensory Receptor Cells, drug effects, Spinal Cord, pathology, TRPV Cation Channels

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          Abstract

          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.

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          Journal
          23704570
          3670709
          10.1126/science.1233765

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