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Targeted ablation, silencing, and activation establish glycinergic dorsal horn neurons as key components of a spinal gate for pain and itch.

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Foster Edmund, Wildner Hendrik, Tudeau Laetitia, Haueter Sabine, Ralvenius William T, Jegen Monika, Johannssen Helge, Hösli Ladina, Haenraets Karen, Ghanem Alexander, Conzelmann Karl-Klaus, Bösl Michael, Zeilhofer Hanns Ulrich,
Project Dorsal Horn Neuronal Circuits Processing Itch
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Original article (peer-reviewed)

Journal Neuron
Volume (Issue) 85(6)
Page(s) 1289 - 304
Title of proceedings Neuron
DOI 10.1016/j.neuron.2015.02.028

Open Access

Abstract

The gate control theory of pain proposes that inhibitory neurons of the spinal dorsal horn exert critical control over the relay of nociceptive signals to higher brain areas. Here we investigated how the glycinergic subpopulation of these neurons contributes to modality-specific pain and itch processing. We generated a GlyT2::Cre transgenic mouse line suitable for virus-mediated retrograde tracing studies and for spatially precise ablation, silencing, and activation of glycinergic neurons. We found that these neurons receive sensory input mainly from myelinated primary sensory neurons and that their local toxin-mediated ablation or silencing induces localized mechanical, heat, and cold hyperalgesia; spontaneous flinching behavior; and excessive licking and biting directed toward the corresponding skin territory. Conversely, local pharmacogenetic activation of the same neurons alleviated neuropathic hyperalgesia and chloroquine- and histamine-induced itch. These results establish glycinergic neurons of the spinal dorsal horn as key elements of an inhibitory pain and itch control circuit.
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