Conditional GSK3ß deletion in parvalbumin-expressing interneurons potentiates excitatory synaptic function and learning in adult mice.
Prog Neuropsychopharmacol Biol Psychiatry
; 100: 109901, 2020 06 08.
Article
en En
| MEDLINE
| ID: mdl-32113851
ABSTRACT
Glycogen synthase kinase 3ß (GSK3ß) has gained interest regarding its involvement in psychiatric and neurodegenerative disorders. Recently GSK3 inhibitors were highlighted as promising rescuers of cognitive impairments for a gamut of CNS disorders. Growing evidence supports that fast-spiking parvalbumin (PV) interneurons are critical regulators of cortical computation. Albeit, how excitatory receptors on PV interneurons are regulated and how this affects cognitive function remains unknown. To address these questions, we have generated a novel triple-transgenic conditional mouse with GSK3ß genetically deleted from PV interneurons. PV-GSK3ß-/- resulted in increased excitability and augmented excitatory synaptic strength in prefrontal PV interneurons. More importantly, these synaptic changes are correlated with accelerated learning with no changes in locomotion and sociability. Our study, for the first time, examined how GSK3ß activity affects learning capability via regulation of PV interneurons. This study provides a novel insight into how GSK3ß may contribute to disorders afflicted by cognitive deficits.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Parvalbúminas
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Sinapsis
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Potenciales Postsinápticos Excitadores
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Glucógeno Sintasa Quinasa 3 beta
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Interneuronas
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Aprendizaje
Límite:
Animals
Idioma:
En
Revista:
Prog Neuropsychopharmacol Biol Psychiatry
Año:
2020
Tipo del documento:
Article
País de afiliación:
Estados Unidos