All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity.
Animals
C-Reactive Protein
/ metabolism
Dominance, Ocular
Interneurons
/ cytology
Mice
Mice, Inbred C57BL
Nerve Tissue Proteins
/ metabolism
Neural Inhibition
Neuronal Plasticity
Parvalbumins
/ metabolism
Pyramidal Cells
/ cytology
Receptors, AMPA
/ metabolism
Receptors, N-Methyl-D-Aspartate
/ metabolism
Visual Cortex
/ physiology
NPTX2
disinhibition
neuropentraxin2
synaptic plasticity
visual cortex
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
14 09 2021
14 09 2021
Historique:
accepted:
07
08
2021
entrez:
11
9
2021
pubmed:
12
9
2021
medline:
15
12
2021
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 34508001
pii: 2105388118
doi: 10.1073/pnas.2105388118
pmc: PMC8449314
pii:
doi:
Substances chimiques
Nerve Tissue Proteins
0
Parvalbumins
0
Receptors, AMPA
0
Receptors, N-Methyl-D-Aspartate
0
neuronal pentraxin
0
C-Reactive Protein
9007-41-4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NINDS NIH HHS
ID : R01 NS036715
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY012124
Pays : United States
Organisme : NINDS NIH HHS
ID : R35 NS097966
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG009973
Pays : United States
Organisme : NIH HHS
ID : S10 OD025223
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY016431
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY025922
Pays : United States
Déclaration de conflit d'intérêts
The authors declare no competing interest.
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