The organization and development of cortical interneuron presynaptic circuits are area specific.
Animals
Cerebral Cortex
/ metabolism
Female
Fragile X Mental Retardation Protein
/ physiology
Fragile X Syndrome
/ genetics
Interneurons
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Neural Pathways
Presynaptic Terminals
/ metabolism
Rabies virus
/ genetics
Sense Organs
/ metabolism
Synapses
/ metabolism
ALM
GABAergic interneurons
cortical areas
development
fragile X syndrome
monosynaptic rabies tracing
sensory cortex
thalamocortical input
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
09 11 2021
09 11 2021
Historique:
received:
26
05
2021
revised:
17
08
2021
accepted:
21
10
2021
entrez:
10
11
2021
pubmed:
11
11
2021
medline:
19
2
2022
Statut:
ppublish
Résumé
Parvalbumin and somatostatin inhibitory interneurons gate information flow in discrete cortical areas that compute sensory and cognitive functions. Despite the considerable differences between areas, individual interneuron subtypes are genetically invariant and are thought to form canonical circuits regardless of which area they are embedded in. Here, we investigate whether this is achieved through selective and systematic variations in their afferent connectivity during development. To this end, we examined the development of their inputs within distinct cortical areas. We find that interneuron afferents show little evidence of being globally stereotyped. Rather, each subtype displays characteristic regional connectivity and distinct developmental dynamics by which this connectivity is achieved. Moreover, afferents dynamically regulated during development are disrupted by early sensory deprivation and in a model of fragile X syndrome. These data provide a comprehensive map of interneuron afferents across cortical areas and reveal the logic by which these circuits are established during development.
Identifiants
pubmed: 34758329
pii: S2211-1247(21)01472-8
doi: 10.1016/j.celrep.2021.109993
pmc: PMC8832360
mid: NIHMS1756262
pii:
doi:
Substances chimiques
Fmr1 protein, mouse
0
Fragile X Mental Retardation Protein
139135-51-6
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
109993Subventions
Organisme : NIMH NIH HHS
ID : R01 MH071679
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH095147
Pays : United States
Organisme : NIMH NIH HHS
ID : R37 MH071679
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS081297
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS039007
Pays : United States
Organisme : NINDS NIH HHS
ID : P01 NS074972
Pays : United States
Informations de copyright
Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests Gord Fishell is a founder of Regel Therapeutics, which has no competing interests with the present manuscript.
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