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LCM-RNAseq on human pyramidal neurons and parvalbumin interneurons from frontal cortex

ABSTRACT: LCM-RNAseq on human pyramidal neurons and parvalbumin interneurons from frontal cortex

PROVIDER: PRJNA627475 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11590661_1.fastq.gz	Fastqsanger.gz
	SRR11590661_2.fastq.gz	Fastqsanger.gz
	SRR11590662_1.fastq.gz	Fastqsanger.gz
	SRR11590662_2.fastq.gz	Fastqsanger.gz
	SRR11590663_1.fastq.gz	Fastqsanger.gz

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LCM-RNAseq on human pyramidal neurons and parvalbumin interneurons from frontal cortex

Project description:Pyramidal neurons and aggregcan-positive interneurons were collected from healthy control human post-mortem brain tissue (Brodmann Area 9) by laser capture microdissection. RNA was collected from pooled cells from 4 donors, and compared with full stained sections to determine enriched genes expressed in each cell type by RNAseq.

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Discrete hippocampal projections are differentially regulated by parvalbumin and somatostatin interneurons

Project description:People with schizophrenia show hyperactivity in the ventral hippocampus (vHipp) and we have previously demonstrated distinct behavioral roles for vHipp cell populations. Here, we test the hypothesis that parvalbumin (PV) and somatostatin (SST) interneurons differentially innervate and regulate hippocampal pyramidal neurons based on their projection target. First, we use eGRASP to show that PV-positive interneurons form a similar number of synaptic connections with pyramidal cells regardless of their projection target while SST-positive interneurons preferentially target nucleus accumbens (NAc) projections. To determine if these anatomical differences result in functional changes, we used in vivo opto-electrophysiology to show that SST cells also preferentially regulate the activity of NAc-projecting cells. These results suggest vHipp interneurons differentially regulate that vHipp neurons that project to the medial prefrontal cortex (mPFC) and NAc. Characterization of these cell populations may provide potential molecular targets for the treatment schizophrenia and other psychiatric disorders associated with vHipp dysfunction.

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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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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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Chronic nicotine differentially affects murine transcriptome profiling in isolated cortical interneurons and pyramidal neurons

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Project description:The mammalian cerebral cortex comprises a complex neuronal network that maintains a delicate balance between excitatory neurons and inhibitory interneurons. Previous studies, including our own research, have shown that specific interneuron subtypes are closely associated with particular pyramidal neuron types, forming stereotyped local inhibitory microcircuits. However, the developmental processes that establish these precise networks are not well understood. Here we show that pyramidal neuron types are instrumental in maintaining the terminal differentiation and survival of specific associated interneuron subtypes. In a wild-type cortex, the relative abundance of different interneuron subtypes aligns precisely with the pyramidal neuron types with which they synaptically target. In Fezf2 mutant cortex, characterized by the absence of layer 5 pyramidal tract neurons and an expansion of layer 6 intratelencephalic neurons, we observed a corresponding decrease in associated layer 5b interneurons and an increase in layer 6 subtypes. Interestingly, these shifts in composition are achieved through mechanisms that are specific to different interneuron types. While SST interneurons adjust their abundance to the change in pyramidal neuron prevalence through the regulation of programmed cell death, parvalbumin cells alter their identity. These findings illustrate two key strategies by which the dynamic interplay between pyramidal neurons and interneurons allows local microcircuits to be sculpted precisely. These insights underscored the precise roles of extrinsic signals from pyramidal cells in the establishment of interneuron diversity and their subsequent integration into local cortical microcircuits.

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Project description:The medial prefrontal cortex (mPFC) is a key brain region involved in controlling working memory, executive function, and self-regulatory behaviours, and its malfunction is a hallmark of several neuropsychiatric disorders such as schizophrenia, depression, and post-traumatic stress disorder. One of the main risk factors for the development of mental illness is chronic stress (CS). Despite some evidence pointing to possible excitation-inhibition (E/I) imbalances caused by CS, the precise mechanism by which CS triggers mPFC dysfunction is not fully understood. Here, using neuroproteomics analysis and whole-cell patch-clamp recordings, we investigated the functional changes in E/I ratio and synaptic drive onto pyramidal neurons and parvalbumin interneurons (PV) in the prelimbic (PL) and infralimbic (IL) cortices, following exposure to 21 days of chronic unpredictable stress. We demonstrate that CS impacts PL- versus IL-pyramidal neurons differently, driving a common decrease in E/I ratio without affecting PV interneurons. Our work brings insightful information and corroborates the hypothesis of stress-induced hypofunction of the mPFC.

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Transcriptomic changes in parvalbumin positive interneurons from cortex and striatum.

Project description:This experiment was designed to compare the transcriptomic differences between two parvalbumin (PV) interneuron population of the mouse brain. These two populations have the same embryological origin and share several neurochemical and electrophysiological properties, but differ in their ability to express the glial cell line-derived neurotrophic factor GDNF (negative in cortex and positive in striatum). Two different reporters for PV expressing cells were used: i) a constitutive tdTomato gene inserted in the Pvalb locus, and ii) a PV-Cre; tdTomato model in which fluorescent cells are PV cells expressing Cre recombinase. The comparative gene expression analysis between PV neurons captured from striatum and cortex allowed unraveling differential molecular characteristics of GDNF-synthesizing striatal PV interneurons and their potential role in endogenous GDNF modulation. The specific expression of several genes of interest in the striatal PV interneurons has been validated by other methods (real-time RT-PCR, in situ hibridization, immunohistochemistry).

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DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

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