Activation of acid‐sensing ion channels by carbon dioxide regulates amygdala synaptic protein degradation in memory reconsolidation

Boren Lin, Khaled Alganem, Sinead M. O’Donovan, Zhen Jin, Farzaneh Sadat Naghavi, Olivia A. Miller, Tyler C. Ortyl, Ye Chun Ruan, Robert E. McCullumsmith, Jianyang Du

Research output: Journal article publicationJournal articleAcademic researchpeer-review

3 Citations (Scopus)


Reconsolidation has been considered a process in which a consolidated memory is turned into a labile stage. Within the reconsolidation window, the labile memory can be either erased or strengthened. Manipulating acid-sensing ion channels (ASICs) in the amygdala via carbon dioxide (CO2) inhalation enhances memory retrieval and its lability within the reconsolidation window. Moreover, pairing CO2 inhalation with retrieval bears the reactivation of the memory trace and enhances the synaptic exchange of the calcium-impermeable AMPA receptors to calcium-permeable AMPA receptors. Our patch-clamp data suggest that the exchange of the AMPA receptors depends on the ubiquitin-proteasome system (UPS), via protein degradation. Ziram (50 µM), a ubiquitination inhibitor, reduces the turnover of the AMPA receptors. CO2 inhalation with retrieval boosts the ubiquitination without altering the proteasome activity. Several calcium-dependent kinases potentially involved in the CO2-inhalation regulated memory liability were identified using the Kinome assay. These results suggest that the UPS plays a key role in regulating the turnover of AMPA receptors during CO2 inhalation.

Original languageEnglish
Pages (from-to)78-78
Number of pages1
JournalMolecular Brain
Issue number1
Publication statusPublished - 7 May 2021


  • Acid‐sensing ion channels
  • AMPA receptors
  • Aversive conditioning
  • Carbon dioxide
  • Memory retrieval
  • Proteasome
  • Protein degradation
  • Reconsolidation
  • Ubiquitination

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience


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