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A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons.

ABSTRACT: A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons.

PROVIDER: PRJNA1079679 | ENA |

REPOSITORIES: ENA

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A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons [CUT&RUN]

Project description:Cortical neurons are specified during embryonic development but often only acquire their mature properties at relatively late stages of postnatal development. This delay in terminal differentiation is particularly prominent for fast-spiking parvalbumin-expressing (PV+) interneurons, which play critical roles in regulating the activity of the cerebral cortex. We found that the terminal differentiation of PV+ interneurons is triggered by neuronal activity and mediated by the transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1a). Developmental loss of PGC-1a prevents PV+ interneurons from acquiring their unique structural, electrophysiological, synaptic, and metabolic features and disrupts PV+ interneuron subtype specification. PGC-1a exerts its function as a master regulator of the differentiation of PV+ interneurons by directly controlling gene expression through a transcriptional complex that includes ERRg and Mef2c. Our results uncover a molecular switch that translates neural activity into transcriptional programs promoting the maturation of PV+ interneurons at the appropriate developmental stage.

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A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons [scRNA-seq]

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A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons [scRNA-seq]

Project description:A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons [scRNA-seq]

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DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

Project description:Our group has reported that the histone methyltransferase DOT1L is necessary for proper cortical plate development and layer distribution of glutamatergic neurons, however, its specific role on cortical interneuron development has not yet been explored. Here, we demonstrate that DOT1L affects interneuron development in a cell-autonomous manner. Deletion of Dot1l in MGE-derived interneuron precursor cells results in an overall reduction and altered distribution of GABAergic interneurons in the cortical plate at postnatal day (P) 0. Furthermore, we observed an altered proportion of GABAergic interneurons in the cortex and striatum at P21 with a significant decrease in Parvalbumin (PVALB)-expressing interneurons. Altogether, our results indicate that reduced numbers of cortical interneurons upon DOT1L deletion results from altered postmitotic differentiation/maturation.

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Disruption of KCC2 in parvalbumin-positive interneurons causes fatal epilepsy in mice

Project description:Since many years, we are interested in the regulation of the intraneuronal chloride concentration. We were the first group reporting a full knockout of the KCl-co-transporter KCC2, which dies immediately after birth due to respiratory failure. Notably, KCC2 loss-of-function mutations are associated with inherited febrile seizures, severe genetic generalized epilepsy and epilepsy of infancy with migrating focal seizures. Here, we used our floxed line to study the consequences of the disruption of KCC2 within parvalbumin-positive interneurons in mice. Remarkably, this leads to the disinhibition of PV-positive interneurons as evidenced by a decrease of E-S-Coupling and an increase in the sIPSC frequency. Nevertheless, these mice develop fatal epilepsy with progressive loss of parvalbumin-positive interneurons thus increasing network excitability.

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A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons.

Project description:This SuperSeries is composed of the SubSeries listed below.

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