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

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

PROVIDER: PRJNA1079685 | 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.

2025-07-15 | GSE256442 | GEO

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

2025-07-15 | GSE256441 | GEO

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

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

| PRJNA1079679 | ENA

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]

| PRJNA1079686 | ENA

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.

2022-11-02 | E-MTAB-11147 | biostudies-arrayexpress

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.

2023-08-01 | GSE221994 | GEO

Postnatal loss of Arx transcriptional activity in parvalbumin interneurons induces epilepsy-like network abnormalities

Project description:Postnatal loss of Arx transcriptional activity in parvalbumin interneurons induces epilepsy-like network abnormalities

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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.

2025-07-15 | GSE256443 | GEO

Autophagy is dispensable for the maintenance of parvalbumin interneurons but required for their inhibitory neurotransmission and memory

Project description:Previous studies have demonstrated the requirement of autophagy for neuronal survival and synaptic function, mostly focusing on projection neurons and excitatory neurotransmission. Here, we examine the effects of conditional atg5 ablation in neurons expressing parvalbumin (PV-cKO), which in the forebrain mainly represent fast-spiking inhibitory interneurons. Contrary to the prevailing view, we show that autophagy-deficient PV neurons survive throughout the brain, with the exception of the projection Purkinje neurons in the cerebellum, which rapidly degenerate. While not affecting their maintenance, autophagy deficiency leads to aberrant proteostasis of key synaptic and other proteins, culminating to reduced inhibitory neurotransmission in hippocampal PV-interneurons. Consistently, PV-cKO animals exhibit associative and recognition memory deficits. Our findings demonstrate a neuronal type-specific vulnerability to autophagy deficiency, while also identifying PV-interneurons as the cellular substrates where autophagy is required for memory formation.

2026-02-02 | PXD035264 | Pride

Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer’s disease [GeoMx]

Project description:Alzheimer’s disease is a debilitating neurodegenerative disorder with no cure and few treatment options. In early stages of Alzheimer’s disease, impaired metabolism and functional connectivity of the retrosplenial cortex strongly predict future cognitive impairments. Therefore, understanding Alzheimer’s disease-related deficits in the retrosplenial cortex is critical for understanding the origins of cognitive impairment and identifying early treatment targets. Using the 5xFAD mouse model, we discovered early, sex-dependent alterations in parvalbumin-interneuron transcriptomic profiles. This corresponded with impaired parvalbumin-interneuron activity, which was sufficient to induce cognitive impairments and dysregulate retrosplenial functional connectivity. In fMRI scans from patients with mild cognitive impairment and Alzheimer’s disease, we observed a similar sex-dependent dysregulation of retrosplenial cortex functional connectivity and, in post-mortem tissue from subjects with Alzheimer’s disease, a loss of parvalbumin interneurons. Reversal of cognitive deficits by stimulation of parvalbumin interneurons in the retrosplenial cortex suggests that this may serve as a promising novel therapeutic strategy.

2025-04-13 | GSE277793 | GEO

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