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Df(h15q13)/+ mouse model reveals loss of astrocytes and synaptic-related changes of the excitatory and inhibitory circuits in the medial prefrontal cortex.

ABSTRACT: Df(h15q13)/+ mouse model reveals loss of astrocytes and synaptic-related changes of the excitatory and inhibitory circuits in the medial prefrontal cortex.

PROVIDER: PRJNA613469 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11351583.fastq.gz	Fastqsanger.gz
	SRR11351584.fastq.gz	Fastqsanger.gz
	SRR11351585.fastq.gz	Fastqsanger.gz
	SRR11351586.fastq.gz	Fastqsanger.gz
	SRR11351587.fastq.gz	Fastqsanger.gz

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Df(h15q13)/+ mouse model reveals loss of astrocytes and synaptic-related changes of the excitatory and inhibitory circuits in the medial prefrontal cortex.

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Medial prefrontal cortex (mPFC) transcriptome analysis of Shank3-overexpressing mice

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GluN2D-mediated excitatory drive onto medial prefrontal cortical PV+ fast-spiking inhibitory interneurons.

Project description:Deficits in fast-spiking inhibitory interneurons (FSINs) within the dorsolateral prefrontal cortex (dlPFC) are hypothesized to underlie cognitive impairment associated with schizophrenia. Though representing a minority of interneurons, this key cell type coordinates broad neural network gamma-frequency oscillations, associated with cognition and cognitive flexibility. Here we report expression of GluN2D mRNA selectively in parvalbumin positive cells of human postmortem dlPFC tissue, but not pyramidal neurons, with little to no GluN2C expression in either cell type. In acute murine mPFC slices the GluN2C/D selective positive allosteric modulator (PAM), CIQ(+), increased the intrinsic excitability as well as enhanced NMDAR-mediated EPSCs onto FSINs. This increase in intrinsic excitability with GluN2C/D PAM was also observed in the Dlx 5/6+/- FSIN developmental deficit model with reported FSIN hypoexcitability. Together these data speak to selective modulation of FSINs by a GluN2D PAM, providing a potential mechanism to counter the FSIN-deficit seen in schizophrenia.

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Inhibitory and excitatory responses in the dorso-medial prefrontal cortex during threat processing.

Project description:ObjectiveTo evaluate cortical excitability during instructed threat processing.MethodsSingle and paired transcranial magnetic stimulation (TMS) pulses were applied to the right dorsomedial prefrontal cortex (dmPFC) during high-density electroencephalography (EEG) recording in young healthy participants (n = 17) performing an instructed threat paradigm in which one of two conditioned stimuli (CS+ but not CS-) was paired with an electric shock (unconditioned stimulus [US]). We assessed TMS-induced EEG responses with spectral power (both at electrode and source level) and information flow (effective connectivity) using Time-resolved Partial Directed Coherence (TPDC). Support vector regression (SVR) was used to predict behavioral fear ratings for CS+ based on TMS impact on excitability.ResultsDuring intracortical facilitation (ICF), frontal lobe theta power was enhanced for CS+ compared to single pulse TMS for the time window 0-0.5 s after TMS pulse onset (t(16) = 3.9, p < 0.05). At source level, ICF led to an increase and short intracortical inhibition (SICI) to a decrease of theta power in the bilateral dmPFC, relative to single pulse TMS during 0-0.5 s. Compared to single pulse TMS, ICF increased information flows, whereas SICI reduced the information flows in theta band between dmPFC, amygdala, and hippocampus (all at p < 0.05). The magnitude of information flows between dmPFC to amygdala and dmPFC to hippocampus during ICF (0-0.5 s), predicted individual behavioral fear ratings (CS+; coefficient above 0.75).ConclusionDistinct excitatory and inhibitory mechanisms take place in the dmPFC. These findings may facilitate future research attempting to investigate inhibitory/facilitatory mechanisms alterations in psychiatric disorders and their behavioral correlates.

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Engrailed transcription factors direct embryonic medial excitatory cerebellar nuclei neuron identity and survival

Project description:In the cerebellum, the excitatory neurons of the three cerebellar nuclei (eCN) form the primary output for the circuit. The medial eCN (eCNm) were recently divided into molecularly defined subdomains in the adult, however how they are established during development is not known. We define molecular subdomains of the eCNm using scRNA-seq and spatial expression analysis during embryogenesis. Our analysis shows that the eCNm are transcriptionally divergent from the rest of the eCN by E14.5. We previously showed that conditional loss of the homeobox genesEn1andEn2leads to death of a subset of embryonic eCNm. We demonstrate that loss ofEn1/2in embryonic eCNm results in cell death of a specific posterior eCNm molecular subdomain and loss of TBR2 expression in an anterior subdomain, as well as reduced synaptic gene expression. We further reveal a similar function for EN1/2 in mediating TBR2 expression, neuron differentiation and survival in the two other cerebellar excitatory neuron types. Thus, our work defines embryonic eCNm molecular diversity and reveals conserved roles for EN1/2 in the cerebellar excitatory neuron lineage.

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Single cell transcriptomic and chromatin profiles suggest Layer Vb is the only layer with shared excitatory cell types in the medial and lateral entorhinal cortex

Project description:All brain functionality arises from the activity in neural circuits in different anatomical regions. These regions contain different circuits comprising unique cell types. An integral part to understanding neural circuits is a full census of the constituent parts, i.e., the neural cell types. This census can be based on different characteristics. Previously combinations of morphology and physiology, gene expression, and chromatin accessibility have been used in various cortical and subcortical regions. This has given an extensive yet incomplete overview of neural cell types. However, these techniques have not been applied to all brain regions. Here we apply single cell analysis of accessible chromatin on two similar but different cortical regions, the medial and the lateral entorhinal cortices. Even though these two regions are anatomically similar, their intrinsic and extrinsic connectivity are different. In 4136 cells we identify 20 different clusters representing different cell types. As expected, excitatory cells show regionally specific clusters, whereas inhibitory neurons are shared between regions. We find that several deep layer excitatory neuronal cell types as defined by chromatin profile are also shared between the two different regions. Integration with a larger scRNA-seq dataset maintains this shared characteristic for cells in Layer Vb. Interestingly, this Layer contains three clusters, two specific to either subregion and one shared between the two. These clusters can be putatively associated with particular functional and anatomical cell types found in this layer. This information is a step forwards into elucidating the cell types within the entorhinal circuit and by extension its functional underpinnings.

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