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Expression data of hippocampal CA3 from Adora1 knockout and wild type mice

ABSTRACT: Expression data of hippocampal CA3 from Adora1 knockout and wild type mice

PROVIDER: PRJNA798039 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17645825.fastq.gz	Fastqsanger.gz
	SRR17645826.fastq.gz	Fastqsanger.gz
	SRR17645827.fastq.gz	Fastqsanger.gz
	SRR17645828.fastq.gz	Fastqsanger.gz
	SRR17645829.fastq.gz	Fastqsanger.gz

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Expression data of hippocampal CA3 from Adora1 knockout and wild type mice

Project description:Purpose: The goals of this study are to analyze the mRNAs expression in hippocampal CA3 after Adora1 knockout by High-throughput sequencing. Methods: The brain was dissected and followed by 20 μm cryosection onto 20 glass slides. The hippocampus CA3 was isolated from brain slides by using laser capture microdissection. Then the samples were stored on dry ice until RNA extraction by Trizol. The RNAseq was conducted by using Illumina HiSeq2000 platform. Results: By performing RNA sequencing on RNAs isolated from the hippocampus CA3 neurons of AKO and C57 mice at 3-month-old. We found that 51 mRNAs were upregulated, whereas 77 mRNAs were downregulated in AKO mice. Conclusion:We deciphered the underlying neuroprotective mechanisms of A1R knockdown in AD mouse models. By employing the RNA-seq technique, we compared the alterations in gene expression in the hippocampus between AKO and wild-type mice.

2022-01-20 | GSE193826 | GEO

Study evaluating striatal and hippocampal tissues between Helios full knockout and wild type mice

Project description:Striatal and hippocampal tissues were dissected out from wild type and helios knockout mice to perform comparisions by pairs of genotypes. First the comparision between wild type and helios knockout mice using striatal tissues and the second comparision was made between wild type and helios knockout hippocampal tissues

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Project description:Despite widespread interest in using human stem cells in neurological disease modeling, a suitable model system to study human neuronal connectivity is lacking. Here, we report a protocol for efficient differentiation of hippocampal pyramidal neurons and an in vitro model for hippocampal neuronal connectivity. We developed an embryonic stem cell (ESC)- and induced pluripotent stem cell (iPSC)-based protocol to differentiate human CA3 pyramidal neurons from patterned hippocampal neural progenitor cells (NPCs). This differentiation induces a comprehensive patterning and generates multiple CA3 neuronal subtypes. The differentiated CA3 neurons are functionally active and readily form neuronal connection with dentate granule (DG) neurons in vitro, recapitulating the synaptic connectivity within the hippocampus. When we applied this neuronal co-culture approach to study connectivity in schizophrenia, we found deficits in spontaneous activity in patient iPSC derived DG–CA3 co-culture by multi-electrode array recording. In addition, both multi-electrode array recording and whole cell patch clamp electrophysiology revealed a reduction in spontaneous and evoked neuronal activity in CA3 neurons derived from schizophrenia patients. Altogether these results underscore the relevance of this new model in studying diseases with hippocampal vulnerability.

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Project description:Aging is associated with a decline in hippocampal mediated learning and memory, a process wich can be ameliorated by dietary (caloric) restriction. We used Affymetrix gene expression analysis to monitor changes in three regions of the hippocampus (CA1, CA3, DG) of middle aged (18 months) and old (28 month) rats that were exposed to dietary restriction. Old rats were determined to be good performers (GP) or poor performers (PP) in behavioral tests to assess thier hippocampal function.

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Project description:Aging is associated with a decline in hippocampal mediated learning and memory, a process which can be ameliorated by dietary (caloric) restriction. We used Affymetrix gene expression analysis to monitor changes in three regions of the hippocampus (CA1, CA3, DG) of middle aged (18 months) and old (28 month) rats that were exposed to dietary restriction. Old rats were determined to be good performers (GP) or poor performers (PP) in behavioural tests to assess their hippocampal function. We used Affymetrix gene expression analysis to monitor changes in three regions of the hippocampus (CA1, CA3, DG) of middle aged (18 months) and old (28 month) rats that were exposed to dietary restriction.

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Project description:Intellectual disability (ID) affects ~2% of the population and ID-associated genes are enriched for epigenetic factors, including those encoding the largest family of histone lysine acetyltransferases (KAT5-KAT8). Among them is KAT6A, whose mutations cause KAT6A Syndrome, with ID as a common clinical feature. However, the underlying molecular mechanism remains unknown. Here, we find that KAT6A deficiency impairs synaptic structure and plasticity in hippocampal CA3, but not in CA1 region, resulting in memory deficits in mice. We further identify a CA3-enriched gene Rspo2, encoding Wnt activator R-spondin 2, as a key transcriptional target of KAT6A. Importantly, deletion of Rspo2 in excitatory neurons impairs memory formation, and restoring RSPO2 expression in CA3 rescues the deficits in Wnt signaling and learning-associated behaviors in Kat6a mutant mice. Collectively, our results demonstrate that KAT6A-RSPO2-Wnt signaling plays a critical role in regulating hippocampal CA3 synaptic plasticity and cognitive function, providing potential therapeutic targets for KAT6A Syndrome and related neurodevelopmental diseases.

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Hippocampal CA3 Transcriptome Signature and Dentate Gyrus MRI Features Correlate with Initial Precipitating Injury in Refractory Temporal Lobe Epilepsy

Project description:We analyzed the transcriptomic profile of CA3 explants surgically obtained from patients with refractory MTLE (mesial temporal lobe epilepsy) and HS (hippocampal sclerosis) in order to investigate if the initial precipitating injury (IPI) influences the molecular mechanisms underlying this condition. CA3 transcriptomic profile was found to be significantly different in cases with prolonged febrile seizures as the IPI (identified here as FS) when compared to correspondent data from cases without febrile seizure history (NFS). CA3 transcriptomic profiles of FS and NFS were compared in order to identify differentially expressed transcripts

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