| First Author | Monaco SA | Year | 2020 |
| Journal | Prog Neuropsychopharmacol Biol Psychiatry | Volume | 100 |
| Pages | 109901 | PubMed ID | 32113851 |
| Mgi Jnum | J:325523 | Mgi Id | MGI:6714512 |
| Doi | 10.1016/j.pnpbp.2020.109901 | Citation | Monaco SA, et al. (2020) Conditional GSK3beta deletion in parvalbumin-expressing interneurons potentiates excitatory synaptic function and learning in adult mice. Prog Neuropsychopharmacol Biol Psychiatry 100:109901 |
| abstractText | Glycogen synthase kinase 3beta (GSK3beta) 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 GSK3beta genetically deleted from PV interneurons. PV-GSK3beta(-/-) 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 GSK3beta activity affects learning capability via regulation of PV interneurons. This study provides a novel insight into how GSK3beta may contribute to disorders afflicted by cognitive deficits. |
