Cell type-specific transcriptional programs in mouse prefrontal cortex during adolescence and addiction
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA514448 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8433700.fastq.gz | Fastqsanger.gz | |||
| SRR8433691.fastq.gz | Fastqsanger.gz | |||
| SRR8433701.fastq.gz | Fastqsanger.gz | |||
| SRR8433692.fastq.gz | Fastqsanger.gz | |||
| SRR8433702.fastq.gz | Fastqsanger.gz |
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Project description:Coordinated activity-induced transcriptional changes across multiple neuron subtypes of the prefrontal cortex (PFC) play a pivotal role in encoding and regulating major cognitive behaviors. Yet, the specific transcriptional programs in each neuron subtype remain unknown. Using single-cell RNA sequencing (scRNA-seq), here we comprehensively classified all unique cell subtypes in the PFC. We analyzed transcriptional dynamics of each cell subtype under a naturally adaptive and an induced condition. Adaptive changes during adolescence (between P21 and P60), a highly dynamic phase of postnatal neuroplasticity, profoundly impacted transcription in each neuron subtype, including cell type-specific regulation of genes implicated in major neuropsychiatric disorders. On the other hand, an induced plasticity evoked by chronic cocaine addiction resulted in progressive transcriptional changes in multiple neuron subtypes and became most pronounced upon prolonged drug withdrawal. Our findings lay a foundation for understanding cell type-specific postnatal transcriptional dynamics under normal PFC function and in neuropsychiatric disease states.
2019-08-29 | GSE124952 | GEO
Project description:The prefrontal cortex is greatly associated with a wide range of mental health illnesses including schizophrenia, depression, bipolar disorder, anxiety and autism spectrum disorders. It richly expresses neuroreceptors which are the target for typical and atypical antipsychotics. However as the precise mechanism of action of antipsychotic medications are not known, proteomic studies of the effects of antipsychotic drugs on the brain are warranted. In the current study we aimed to characterise protein expression in the adult rodent prefrontal cortex (n=5 per group) following low dose treatment with the atypical antipsychotic Risperidone or saline (control) in adolescence (postnatal days 34-47). The prefrontal cortex was examined by triplicate one hour runs of label-free LC-MS/MS. The raw mass spectral data were analyzed with the MaxQuantTM software. Statistical analysis was carried out using SAS Version 9.1. Functional and pathway analysis was performed with DAVID.nih and Ingenuity Pathway Analysis respectively and the top five most implicated pathways were found to be clathrin mediated endocytosis, the tri cyclic acid cycle, remodelling of epithelial junctions, rho family GTPase signalling and mitochondrial dysfunction.This brief report summarises the proteomic data obtained from the study described, adds to the current repertoire of data available concerning the effects of atypical antipsychotic drugs on the brain and sheds light on their biological mechanisms.
2014-05-13 | PXD000480 | Pride
Project description:Background: The present study investigated a role of proteins from BET family (epigenetic readers) in schizophrenia-like abnormalities in MAM-E17 model of schizophrenia. Methods: An inhibitor of BET proteins, JQ1, was given during adolescence in postnatal days (P) 23-P30, and behavioral response (sensorimotor gating, recognition memory) and prefrontal cortex (mPFC) function (long-term potentiation (LTP), molecular and proteomic studies) were performed in adult males and females. Results: Deficits in sensorimotor gating and recognition memory were observed only in MAM-treated males. However, adolescent JQ1 treatment affected control, but MAM-treated groups in both sexes. Electrophysiological study showed an LTP impairment only in male MAM-treated animals, and JQ1 did not have any effect on LTP in the mPFC. In contrast, MAM did not affect immediate early gene expression (markers of neuronal and synaptic activity), but JQ1 altered them in both sexes. Proteomic study revealed alterations in MAM-treated groups only in males, while JQ1 affected both sexes. Conclusions: Prenatal MAM administration induced schizophrenia-like abnormalities only in males. In contrast, adolescent JQ1 treatment affected both sexes and induced behavioral changes in control groups, altered a markers of neuronal and synaptic activity and proteomic landscape in the mPFC of both groups (VEH- and MAM-treated). Thus, adolescent inhibition of BET family might change neuroplasticity in the mPFC.
2021-09-07 | PXD027050 | Pride
Project description:Abnormal development of the prefrontal cortex (PFC) is associated with a number of neuropsychiatric disorders that have an onset in childhood or adolescence. Although the basic laminar structure of the PFC is established in utero, extensive remodeling continues into adolescence. To map the overall pattern of changes in cortical gene transcripts during post-natal development, we made serial measurements of mRNA levels in mouse PFC using oligonucleotide microarrays. We observed changes in mRNA transcripts consistent with known post-natal morphological and biochemical events. Overall, most transcripts that changed significantly showed a progressive decrease in abundance after birth, with the majority of change between post-natal weeks 2 and 4. Genes with cell proliferative, cytoskeletal, extracellular matrix, plasma membrane lipid / transport, protein folding, and regulatory functions had decreases in mRNA levels. Quantitative PCR verified the microarray results for six selected genes: DNA methyltransferase 3A (Dnmt3a), procollagen, type III, alpha 1 (Col3a1), solute carrier family 16 (monocarboxylic acid transporters), member 1 (Slc16a1), MARCKS-like 1 (Marcksl1), nidogen 1 (Nid1) and 3-hydroxybutyrate dehydrogenase (heart, mitochondrial) (Bdh). Keywords: time course, development, mRNA expression Single-channel affymetrix arrays were used to profile mRNA expression in the prefrontal cortex (PFC) of male mice at different time-points after birth (post-natal). Each array is an independent animal.
2006-05-15 | E-GEOD-4675 | biostudies-arrayexpress
Project description:Coordinated activity-induced transcriptional changes across multiple neuron subtypes of the prefrontal cortex (PFC) play a pivotal role in encoding and regulating major cognitive behaviors. Yet, the specific transcriptional programs in each neuron subtype remain unknown. Using single-cell RNA sequencing (scRNA-seq), here we comprehensively classify all unique cell subtypes in the PFC. We analyze transcriptional dynamics of each cell subtype under a naturally adaptive and an induced condition. Adaptive changes during adolescence (between P21 and P60), a highly dynamic phase of postnatal neuroplasticity, profoundly impacted transcription in each neuron subtype, including cell type-specific regulation of genes implicated in major neuropsychiatric disorders. On the other hand, an induced plasticity evoked by chronic cocaine addiction resulted in progressive transcriptional changes in multiple neuron subtypes and became most pronounced upon prolonged drug withdrawal. Our findings lay a foundation for understanding cell type-specific postnatal transcriptional dynamics under normal PFC function and in neuropsychiatric disease states.
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Project description:Animal models provide opportunity to study neurobiological aspects of human alcoholism. Changes in gene expression have been implicated in mediating brain function, including reward system and addiction. The current study aimed to identify novel genes that may underlie ethanol preference. Microarray analysis comparing gene expression in nucleus accumbens (NAc), hippocampus (HP) and prefrontal medial cortex (mPFC) was performed in two rat strains selected for extreme levels of ethanol preference - Warsaw High Preferring (WHP) and Warsaw Low Preferring (WLP). The identified candidate genes may underlie differential ethanol preference in rat model of alcoholism. This is analysis of 18 RNA samples, including 9 technical replicates. Two strains of rats selected for extreme levels of ethanol preference (low preferring WLP and high preferring WHP) were compared. Three brain areas (nucleus accumbens, prefrontal medial cortex and hippocampus) were studied. For each brain area, 6 RNA samples (including 3 technical replicates) were analyzed. Each RNA sample consist of of equal amounts of total RNA from 3 male rats. Comparisons: Nucleus accumbens of WHP vs. Nucleus accumbens of WLP; Prefrontal medial cortex of WHP vs. Prefrontal medial cortex of WLP; Hippocampus of WHP vs. Hippocampus of WLP. 3 biological replicates in each comparison.
2015-01-17 | E-GEOD-65064 | biostudies-arrayexpress
Project description:Transcriptional study to investigate differences in prefrontal cortex and striatum of mice that consumed ethanol despite negative consequences, which resembles the compulsive aspect of alcohol addiction. The transcriptional analysis performed in the striatum and prefrontal cortex revealed genes and biological pathways differentially regulated specifically in animals of the group Inflexible Drinkers that could be involved with the loss of control over voluntary ethanol consumption (da Silva E Silva et al., 2016; de Paiva Lima et al., 2017).
2018-11-30 | GSE123114 | GEO
Project description:The human brain has changed dramatically since humans diverged from our closest living relatives, chimpanzees and the other great apes. However, the genetic and developmental programs underlying this divergence are not fully understood. Here, we generate single-nucleus RNA-seq data of human, chimpanzee and macaque adult prefrontal cortex. Spatial information is obtained by isolating nuclei from sequential sections sliced from basal to apical positions. By comparing transcriptome of different cell types in the three species, we map human-specific expression in adult prefrontal cortex. By comparing to single cell RNA-seq data of cerebral organoids of the same species, we find developmental differences that persist into adulthood, as well as cell state-specific changes that occur exclusively in the adult brain.
2019-10-04 | E-MTAB-8230 | biostudies-arrayexpress
Project description:Abnormal development of the prefrontal cortex (PFC) is associated with a number of neuropsychiatric disorders that have an onset in childhood or adolescence. Although the basic laminar structure of the PFC is established in utero, extensive remodeling continues into adolescence. To map the overall pattern of changes in cortical gene transcripts during post-natal development, we made serial measurements of mRNA levels in mouse PFC using oligonucleotide microarrays. We observed changes in mRNA transcripts consistent with known post-natal morphological and biochemical events. Overall, most transcripts that changed significantly showed a progressive decrease in abundance after birth, with the majority of change between post-natal weeks 2 and 4. Genes with cell proliferative, cytoskeletal, extracellular matrix, plasma membrane lipid / transport, protein folding, and regulatory functions had decreases in mRNA levels. Quantitative PCR verified the microarray results for six selected genes: DNA methyltransferase 3A (Dnmt3a), procollagen, type III, alpha 1 (Col3a1), solute carrier family 16 (monocarboxylic acid transporters), member 1 (Slc16a1), MARCKS-like 1 (Marcksl1), nidogen 1 (Nid1) and 3-hydroxybutyrate dehydrogenase (heart, mitochondrial) (Bdh). Keywords: time course, development, mRNA expression
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