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Article Dans Une Revue eLife Année : 2022

Centrally expressed Cav3.2 T-type calcium channel is critical for the initiation and maintenance of neuropathic pain

Sophie Fayad
Benjamin Le Gac
  • Fonction : Auteur
Antoine Fruquière
  • Fonction : Auteur
Sophie Laffray
  • Fonction : Auteur
Laila Gasmi
  • Fonction : Auteur
Bruno Cauli
Christophe Mallet
Emmanuel Bourinet
  • Fonction : Auteur
Thomas Bessaih
Régis Lambert
Nathalie Leresche

Résumé

Cav3.2 T-type calcium channel is a major molecular actor of neuropathic pain in peripheral sensory neurons, but its involvement at the supraspinal level is almost unknown. In the anterior pretectum (APT), a hub of connectivity of the somatosensory system involved in pain perception, we show that Cav3.2 channels are expressed in a subpopulation of GABAergic neurons coexpressing parvalbumin (PV). In these PV-expressing neurons, Cav3.2 channels contribute to a high-frequency-bursting activity, which is increased in the spared nerve injury model of neuropathy. Specific deletion of Cav3.2 channels in APT neurons reduced both the initiation and maintenance of mechanical and cold allodynia. These data are a direct demonstration that centrally expressed Cav3.2 channels also play a fundamental role in pain pathophysiology.

Dates et versions

hal-04256569 , version 1 (24-10-2023)

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Citer

Sophie Fayad, Guillaume Ourties, Benjamin Le Gac, Baptiste Jouffre, Sylvain Lamoine, et al.. Centrally expressed Cav3.2 T-type calcium channel is critical for the initiation and maintenance of neuropathic pain. eLife, 2022, 11, ⟨10.7554/eLife.79018⟩. ⟨hal-04256569⟩

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