Transcriptional profiling of interneurons in the cerebral cortex of Htr3a-Cre (NO176) mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA594995 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10673757_1.fastq.gz | Fastqsanger.gz | |||
| SRR10673757_2.fastq.gz | Fastqsanger.gz | |||
| SRR10673758_1.fastq.gz | Fastqsanger.gz | |||
| SRR10673758_2.fastq.gz | Fastqsanger.gz | |||
| SRR10673759_1.fastq.gz | Fastqsanger.gz |
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Project description:TRAP translational profiling is a method that allows investigators to genetically characterize specific cell types in complex tissues such as mouse brain. Using this technique we obtained RNA-Seq data from actively translating transcripts present in interneurons in the cerebral cortex of adult Htr3a-Cre (NO176) mice x Rosa26-LSL-EGFP/Rpl10a mice
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Project description:In the mammalian cerebral cortex, the developmental events governing the allocation of different classes of inhibitory neurons into distinct cortical layers are poorly understood. Here we report that the guidance receptor PlexinA4 is upregulated in serotonin receptor 3a-expressing (HTR3A) cortical interneurons (hINs) as they invade the cortical plate and that it regulates their laminar allocation to superficial cortical layers. We find that the PlexinA4 ligand Semaphorin3A acts as a chemorepulsive factor on hINs migrating into the nascent cortex and demonstrate that Semaphorin3A specifically controls their laminar positioning through PlexinA4. We identify that deep layer interneurons constitute a major source of Semaphorin3A in the developing cortex and demonstrate that cell-type specific genetic deletion of Semaphorin3A in these interneurons specifically affects the laminar allocation of hINs. These data demonstrate that in the neocortex, deep layer interneurons control the laminar allocation of hINs into superficial layers.
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Project description:TRAP translational profiling is a method that allows investigators to genetically characterize specific cell types in complex tissues such as mouse brain. Using this technique we obtained RNA-Seq data from actively translating transcripts present in neurons in the cerebral cortex and dentate gyrus of adult Rbp4-Cre (KL100) mice x Rosa26-LSL-EGFP/Rpl10a mice.
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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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Project description:Inhibitory GABAergic interneurons create different brain activity patterns that correlate with behavioral states. In this characterizing study, we used single-cell RNAseq to analyze anatomically- and electrophysiologically-identified hippocampal oriens-lacunosum moleculare (OLM) interneurons. OLMs express somatostatin (Sst), generate feedback inhibition, and play important roles in theta oscillations and fear encoding. Although an anatomically- and biophysically-homogenous population, OLMs comprise two functionally distinct types with presumed different developmental origins, inferred from the expression pattern of serotonin type-3a (5-HT3a, or Htr3a) receptor subunit and 5-HT-excitability in a set of OLMs. To broadly characterize OLM cells, we used the Sst-Cre and the BAC-transgenic Htr3a-Cre mouse lines and separately analyzed SstCre-OLM and Htr3aCre-OLM types. We found a surprisingly consistent expression of Npy in OLMs, which was previously not associated with the identity of this type. Our analyses furthermore revealed uniform expression of developmental origin-related genes, including transcription factors and neurexin isoforms, without providing support for the current view that OLMs may originate from multiple neurogenic zones. Together, we found that OLMs constitute a highly homogenous transcriptomic population. Finally, our results revealed surprisingly infrequent expression of Htr3a in only ~10% of OLMs, and an apparently specific expression of the 5-HT3b subunit-coding gene Htr3b in Htr3aCre-OLMs, but not in SstCre-OLMs. However, additional in situ hybridization experiments suggested that the differential expression of Htr3b may represent an unexpected consequence arising from the design of the Htr3a-Cre BAC transgenic line.
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Project description:<p><strong>BACKGROUND:</strong> The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.</p><p><strong>METHODS:</strong> We have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.</p><p><strong>RESULTS:</strong> Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), L-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, L-homophenylalanine, oleic acid and ceramide (d18:1/16:0).</p><p><strong>CONCLUSIONS:</strong> Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.</p>
2020-04-23 | MTBLS770 | MetaboLights