All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

Daniel Severin, Su Z. Hong, Seung Eon Roh, Shiyong Huang, Jiechao Zhou, Michelle C.D. Bridi, Ingie Hong, Sachiko Murase, Sarah Robertson, Rebecca P. Haberman, Richard L. Huganir, Michela Gallagher, Elizabeth M. Quinlan, Paul Worley, Alfredo Kirkwood

Research output: Contribution to journalArticlepeer-review


Disinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience. Our investigation on disinhibitory mechanisms in the classical model of ocular dominance plasticity uncovered an unexpected form of experience-dependent circuit plasticity. In the layer 2/3 of mouse visual cortex, monocular deprivation triggers a complete, "all-or-none," elimination of connections from pyramidal cells onto nearby parvalbumin-positive interneurons (Pyr→PV). This binary form of circuit plasticity is unique, as it is transient, local, and discrete. It lasts only 1 d, and it does not manifest as widespread changes in synaptic strength; rather, only about half of local connections are lost, and the remaining ones are not affected in strength. Mechanistically, the deprivation-induced loss of Pyr→PV is contingent on a reduction of the protein neuropentraxin2. Functionally, the loss of Pyr→PV is absolutely necessary for ocular dominance plasticity, a canonical model of deprivation-induced model of cortical remodeling. We surmise, therefore, that this all-or-none loss of local Pyr→PV circuitry gates experience-dependent cortical plasticity.

Original languageEnglish (US)
Article numbere2105388118
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number37
StatePublished - Sep 14 2021


  • Disinhibition
  • NPTX2
  • Neuropentraxin2
  • Synaptic plasticity
  • Visual cortex

ASJC Scopus subject areas

  • General


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