Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA376196 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5277230.fastq.gz | Fastqsanger.gz | |||
| SRR5277231.fastq.gz | Fastqsanger.gz | |||
| SRR5277232.fastq.gz | Fastqsanger.gz | |||
| SRR5277233.fastq.gz | Fastqsanger.gz | |||
| SRR5277234.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Circuit neuroscience has made great progress by linking neuronal function to marker gene expression, allowing the specific investigation of otherwise indistinguishable neuronal ensembles. Here, we performed next generation sequencing on two functionally and genetically distinct interneuronal populations marked by the expression of protein kinase C δ (PKCδ) or somatostatin (SST) in the central amygdala (CEA) of mice, which are known to play distinct and sometimes opposing roles in emotion processing. Making their gene expression profile known will aid in forming hypotheses of how different neurotransmitters or psychoactive drugs could alter information processing in these neurons.
2018-12-26 | GSE95154 | GEO
Project description:Both the amygdala and the bed nucleus of the stria terminalis (BNST) have been implicated in maladaptive anxiety characteristic of anxiety disorders. However, the underlying circuit and cellular mechanisms have remained elusive. Here we show that mice with Erbb4 gene deficiency in somatostatin-expressing (SOM+) neurons exhibit heightened anxiety as measured in the elevated plus maze test and the open field test, two assays commonly used to assess anxiety-related behaviors in rodents. Using a combination of electrophysiological, molecular, genetic and pharmacological techniques we demonstrate that the abnormal anxiety in the mutant mice is caused by enhanced excitatory synaptic inputs onto SOM+ neurons in the central amygdala (CeA), and the resulting reduction in inhibition onto downstream SOM+ neurons in the BNST. Notably, our results indicate that an increase in dynorphin signaling in SOM+ CeA neurons mediates the paradoxical reduction in inhibition onto SOM+ BNST neurons, and that the consequent enhanced activity of SOM+ BNST neurons is both necessary for and sufficient to drive the elevated anxiety. Finally, we show that the elevated anxiety and the associated synaptic dysfunctions and increased dynorphin signaling in the CeA-BNST circuit of the Erbb4 mutant mice can be recapitulated by stress in wild-type mice. Together, our results unravel previously unknown circuit and cellular processes in the central extended amygdala that can cause maladaptive anxiety.
2018-05-31 | GSE113979 | GEO
Project description:A complete cell type census based on their full molecular profiles at subclass level and their subnuclei distribution in the central amygdala (CeA), linked with their behavior relevance, is still lacking. Here, we performed single nuclei RNA sequencing in adult mice and compared the results with known genetic and functionally defined populations. We identified 9 transcriptionally and spatially discrete cell types (3 in the lateral division CeL; 5 in the medial division CeM; and 1 in the capsular division CeC). In the CeL, we found one PKCδ expressing cluster (CeL PKCδ ) and two clusters marked by Sst: the CeL Sst cluster which contains the largest and most highly expressing population of Sst-positive neurons, and the CeL NTS/Tac2 cluster which contains low expressing Sst-positive cells. This two Sst population are also Htr2a positive. The CeC contains one cluster marked by the expression of Calcrl and partially expressed PKCδ. In the CeM, the largest cluster was marked by Il1Rapl2, which contains the CeM subsets of Pnoc and Htr2a, and is likely appetitive. Another Sst population, the CeM Tac1/Sst, remains largely unexplored. Moreover, we discovered three previously uncharacterized CeM clusters: CeM Vdr, CeM Drd2/Rai14, and CeM Dlk1. To begin investigating whether these cell types show individual responses in appetitive behavior, we compared their transcriptomes in food-deprived and satiated mice. We found a cell type specific transcriptional response across neuronal populations, particularly in one of the appetitive clusters in the CeL.
2023-05-06 | GSE231790 | GEO
Project description:The central amygdala (CEA) is a brain region that consists of primarily GABAergic neurons. It has been widely investigated for its role in many innate and adaptive behaviors, such as appetitive and defensive behaviors. Despite the complex functions of CEA, the molecular diversity of CEA neurons has not been systemically examined. Here, we performed single-cell RNA-sequencing (scRNA-Seq) in the CEA to classify the molecularly defined neuron types in this region.
2023-02-03 | GSE213828 | GEO
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 to 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function. Differences in gene expression in the central nucleus of the amygdala (CeA) were compared in two groups of alcohol-preferring (P) rats, one given water only and the other given access to 15 & 30% ethanol during adolescence.
2013-07-20 | E-GEOD-49040 | biostudies-arrayexpress
Project description:Human pancreatic δ cells maintain the balance of pancreatic hormones and loss of δ cells or disruption of somatostatin release is associated with diabetes. Despite their important role, human δ cells are scarce (~5% within the islets), limiting physiological studies and drug discovery targeting δ cells. To date, no directed δ-cell differentiation method has been established. In this study, we established a link between fibroblast growth factor (FGF) signaling pathways and pancreatic δ-cell lineage specification. FGF7 helped maintain a pancreatic endoderm/progenitor state with higher expression levels of PDX1 and CHGA, whereas FGF2 biased cells towards the pancreatic δ-cell lineage by inducing the expression of SST and the δ-cell specific transcription factor HHEX, via FGF receptor 1(FGFR1). We developed a differentiation method to generate δ cells from human stem cells by combining FGF2 with FGF7, which synergistically directs pancreatic lineage differentiation and modulates the expression of transcription factors and SST activators during endoderm/endocrine precursor induction. These δ cells display mature RNA profiles and fine secretory granules, secrete somatostatin in response to various stimuli, and suppress insulin secretion from in vitro co-cultured b cells and mouse b cells upon transplantation. The generation of somatostatin-secreting pancreatic δ cells from human stem cells in vitro would provide an unprecedented cell source for drug discovery and cell transplantation studies in diabetes.
2024-06-18 | GSE269764 | GEO
Project description:Inositol 1,4,5-trisphosphate 3-kinase A (IP3K-A) is a molecule enriched in the brain and neurons that regulates intracellular calcium levels via signaling through the inositol trisphosphate receptor. In the present study, we found that IP3K-A expression is highly enriched in the central nucleus of the amygdala (CeA), which plays a pivotal role in the processing and expression of emotional phenotypes in mammals. We used microarray to identify differentially expressed genes in the amydala of wild type (WT) and IP3K-A KO mice.
2016-01-21 | GSE77001 | GEO
Project description:The goal of this project was to assess how alternative splicing programs are arrayed across neuronal cells types. We systematically mapped ribosome-associated transcript isoforms in genetically-defined neuron types of the mouse forebrain. The endogenous ribosomal protein Rpl22 was conditionally HA-tagged in glutamatergic neurons (using CamK2-cre for most neocortical pyramidal cells and Scnn1a-cre for spiny stellate and star pyramid layer 4 cells), and GABAergic interneurons [with somatostatin-cre (SST), parvalbumin-cre (PV) and vasointestinal peptide-cre (VIP)]. Within the hippocampus, we further targeted Cornu ammonis 1 (CA1) neurons (CamK2-cre), CA3 neurons (Grik4-cre), and SST-positive interneurons (SST-cre). Four replicates were deep sequenced (~100 million reads) using an Illumina platform. We find that neuronal transcript isoform profiles reliably distinguish even closely-related classes of pyramidal cells and inhibitory interneurons in the mouse hippocampus and neocortex, positing transcript diversification by alternative splicing as a central mechanism for the functional specification of neuronal cell types and circuits.
2019-07-01 | GSE133291 | GEO
Project description:The objective of this study was to determine common innate differences in gene expression in the Central Nucleus of the Amygdala (CeA) among the selectively bred (a) alcohol-preferring (P) vs. alcohol-non-preferring (NP) rats: (b) high-alcohol-drinking (HAD) vs. low-alcohol-drinking (LAD) rats (both replicates); (c) ALKO alcohol (AA) vs. nonalcohol (ANA) rats; and (d) Sardinian alcohol-preferring (sP) vs. alcohol-nonpreferring (sNP) rats. Comparison of Differences in Gene Expression in the Central Nucleus of the Amygdala (CeA) of 5 Pairs of Rat Lines Selectively Bred for High or Low Alcohol Consumption.
2012-07-31 | E-GEOD-31708 | biostudies-arrayexpress
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 – 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function. Differences in gene expression in brain nucleus accumbens shell (Acb-sh) were compared in two groups of alcohol-preferring (P) rats, one given water only and the other given access to 15 & 30% ethanol during adolescence.
2013-07-20 | E-GEOD-49041 | biostudies-arrayexpress