Hyperactivity of anterior cingulate cortex areas 24a/24b drives chronic pain-induced anxiodepressive-like consequences

Jim Sellmeijer, Victor Mathis, Sylvain Hugel, U. Hui Li, Qian Song, Qi Yu Chen, Florent Barthas, Pierre Eric Lutz, Meltem Karatas, Andreas Luthi, Pierre Veinante, Ad Aertsen, Michel Barrot, Min Zhuo, Ipek Yalcin

Research output: Contribution to journalArticlepeer-review

135 Scopus citations


Pain associates both sensory and emotional aversive components, and often leads to anxiety and depression when it becomes chronic. Here, we characterized, in a mouse model, the long-term development of these sensory and aversive components as well as anxiodepressive-like consequences of neuropathic pain and determined their electrophysiological impact on the anterior cingulate cortex (ACC, cortical areas 24a/24b). We show that these symptoms of neuropathic pain evolve and recover in different time courses following nerve injury in male mice. In vivo electrophysiological recordings evidence an increased firing rate and bursting activity within the ACC when anxiodepressive-like consequences developed, and this hyperactivity persists beyond the period of mechanical hypersensitivity. Wholecell patch-clamp recordings also support ACC hyperactivity, as shown by increased excitatory postsynaptic transmission and contribution of NMDA receptors. Optogenetic inhibition of the ACC hyperactivity was sufficient to alleviate the aversive and anxiodepressive-like consequences of neuropathic pain, indicating that these consequences are underpinned by ACC hyperactivity.

Original languageEnglish
Pages (from-to)3102-3115
Number of pages14
JournalJournal of Neuroscience
Issue number12
StatePublished - 21 Mar 2018
Externally publishedYes


  • Anterior cingulate cortex
  • Anxiety
  • Depression
  • Electrophysiology
  • Neuropathic pain
  • Optogenetics


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