Cav3.2 T-type calcium channel is a major molecular actor of neuropathic pain in peripheral sensory neurons, but its involvement at the supra-spinal 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 sub-population of GABAergic neurons co-expressing 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.
All data generated or analysed during this study are included in the manuscript and supporting files.
- Emmanuel Bourinet
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Animal experimentation: All procedures complied with the ethical guidelines of the Federation for Laboratory Animal Science Associations (FELASA) and with the approval of the French National Consultative Ethics Committee for health and life sciences (authorization number: 17958).
- Gary L Westbrook, Oregon Health & Science University, United States
- Received: March 28, 2022
- Accepted: November 22, 2022
- Accepted Manuscript published: November 23, 2022 (version 1)
© 2022, Fayad et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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