Expression data from induced parvalbumin neurons.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE79146 | GEO | 2016/03/12
SECONDARY ACCESSION(S): PRJNA315015
REPOSITORIES: GEO
Similar Datasets
Project description:Parvalbumin neurons, as an important subtype of inhibitory neurons, play a crucial role in the brain. The dysfunctions of those cells are associated with multiple neural system disorders. We carried out whole gene expression studies for the induction process of parvalbumin neurons. We used microarrays to detail the global program of gene expression underlying cellularization and identified distinct classes of up-regulated genes during this process. Induced parvalbumin neuron cells were selected at successive stages of induction process for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain homogeneous populations of induced parvalbumin neurons at each developmental stage in order to increase the temporal resolution of expression profiles.
2016-03-12 | E-GEOD-79146 | biostudies-arrayexpress
Project description:Dysregulation of pyramidal cell network function by the soma- and axon-targeting inhibitory neurons that contain the calcium-binding protein parvalbumin (PV) represents a core pathophysiological feature of schizophrenia. In order to gain insight into the molecular basis of their functional impairment, we used laser capture microdissection (LCM) to isolate PV-immunolabeled neurons from layer 3 of BrodmannM-bM-^@M-^Ys area 42 of the superior temporal gyrus (STG) from postmortem schizophrenia and normal control brains. We then extracted ribonucleic acid (RNA) from these neurons and determined their messenger RNA (mRNA) expression profile using the Affymetrix platform of microarray technology. 739 mRNA transcripts were found to be differentially expressed in PV neurons in subjects with schizophrenia, including genes associated with WNT (wingless-type), NOTCH and PGE2 (prostaglandin E2) signaling, in addition to genes that regulate cell cycle and apoptosis. Of these 739 genes, only 89 (12%) were also differentially expressed in pyramidal neurons as found in the accompanying study, suggesting that the molecular pathophysiology of schizophrenia appears to be predominantly neuronal type-specific. Taken together, findings of this study provide a neurobiological framework within which hypotheses of the molecular mechanisms that underlie the dysfunction of PV neurons in schizophrenia can be generated and experimentally explored and, as such, may ultimately inform the conceptualization of targeted molecular intervention. Gene expression microarray from mRNA isolated from parvalbumin cells in layer 3 of the STG from 8 normal controls and 8 subjects with schizophrenia. There was no significant difference between diagnosis groups for age, sex, and post mortem interval (PMI).
2013-05-01 | E-GEOD-46509 | biostudies-arrayexpress
Project description:We report the genome-wide gene expression in parvalbumin neurons in frontal cortex of of Fxr1 knockout mice
2021-08-17 | GSE148890 | GEO
Project description:Dysregulation of pyramidal cell network function by the soma- and axon-targeting inhibitory neurons that contain the calcium-binding protein parvalbumin (PV) represents a core pathophysiological feature of schizophrenia. In order to gain insight into the molecular basis of their functional impairment, we used laser capture microdissection (LCM) to isolate PV-immunolabeled neurons from layer 3 of Brodmann’s area 42 of the superior temporal gyrus (STG) from postmortem schizophrenia and normal control brains. We then extracted ribonucleic acid (RNA) from these neurons and determined their messenger RNA (mRNA) expression profile using the Affymetrix platform of microarray technology. 739 mRNA transcripts were found to be differentially expressed in PV neurons in subjects with schizophrenia, including genes associated with WNT (wingless-type), NOTCH and PGE2 (prostaglandin E2) signaling, in addition to genes that regulate cell cycle and apoptosis. Of these 739 genes, only 89 (12%) were also differentially expressed in pyramidal neurons as found in the accompanying study, suggesting that the molecular pathophysiology of schizophrenia appears to be predominantly neuronal type-specific. Taken together, findings of this study provide a neurobiological framework within which hypotheses of the molecular mechanisms that underlie the dysfunction of PV neurons in schizophrenia can be generated and experimentally explored and, as such, may ultimately inform the conceptualization of targeted molecular intervention.
2013-05-01 | GSE46509 | GEO
Project description:Schizophrenia is associated with dysfunction of the dorsolateral prefrontal cortex (DLPFC). This dysfunction is manifest as cognitive deficits that appear to arise from disturbances in gamma frequency oscillations. These oscillations are generated in DLPFC layer 3 via reciprocal connections between pyramidal cells and parvalbumin (PV)-containing interneurons. The density of cortical PV neurons is not altered in schizophrenia, but expression levels of several transcripts involved in PV cell function, including PV, are lower in the disease.
2018-07-01 | GSE93577 | GEO
Project description:LCM-RNAseq on human pyramidal neurons and parvalbumin interneurons from frontal cortex
| PRJNA627475 | ENA
Project description:Mutations in the X-linked solute carrier family 6-member (Slc6a8) gene, encoding the protein responsible for cellular creatine (Cr) uptake, cause Creatine Transporter Deficiency (CTD), an X-linked neurometabolic disorder presenting with cognitive dysfunction, autistic-like features, and epilepsy. The pathological determinants of CTD are still poorly understood and this lack of knowledge might hinder the development of therapeutic strategies. Here, we show that Cr deficiency perturbs gene expression in excitatory neurons, inhibitory cells and oligodendrocytes, inducing a remodeling of circuit excitability and synaptic wiring, while no effects are present in astrocytes and endothelial cells. We also describe specific alterations of high-energy demanding, Parvalbumin-expressing (PV+) interneurons, exhibiting a reduction in cellular and synaptic density, and a hypofunctional phenotype, affecting initiation, kinetics and frequency of action potentials. Mice lacking Slc6a8 only in PV+ neurons recapitulate numerous CTD features, such as cognitive deterioration, impaired cortical processing and hyperexcitability of brain circuits, demonstrating that Cr deficit in PV+ cells is sufficient to determine the CTD neurological endophenotype. Moreover, a pharmacological treatment targeted to restore the efficiency of PV+ synapses induces a significant improvement of cortical activity in Slc6a8 knock-out animals. Altogether, these data establish that Slc6a8 is critical for the normal function of PV+ interneurons and that a subtle dysfunction of these cells is critical for the disease pathogenesis, suggesting a novel therapeutic venue for CTD.
2023-06-01 | GSE218797 | GEO
Project description:Reprogramming resident glia into functional and subtype-specific neurons in vivo by delivering reprogramming genes directly to the brain provides a step forward towards the possibility of treating brain injuries or diseases. Here, we show that neurons reprogrammed using Ascl1, Lmx1a and Nurr1 functionally mature and integrate into existing brain circuitry, and that the majority of the reprogrammed neurons have properties of fast spiking, parvalbumin-containing interneurons.
2017-08-29 | GSE101091 | GEO
Project description:Neuroanatomists have long speculated that expanded primate brains contain an increased morphological diversity of inhibitory neurons (doi:10.1038/nrn3444, DeFelipe et al.) and recent studies have identified primate-specific neuronal populations at the molecular level(doi:10.1038/s41586-020-2781-z, Krienen et al.). However, we know little about the developmental mechanisms that specify evolutionarily novel cell types in the brain. Here, we reconstructed gene expression trajectories specifying inhibitory neurons spanning the neurogenic period in macaque and mouse by analyzing the transcriptomes of 250,181 cells. We find that the initial classes of inhibitory neurons generated prenatally are largely conserved among mammals. Nonetheless, we identify two contrasting developmental mechanisms for specifying evolutionarily novel cell types during prenatal development. First, we show that recently-identified primate-specific TAC3 striatal interneurons are specified by a unique transcriptional program in progenitors followed by induction of a distinct suite of neuropeptides and neurotransmitter receptors in newborn neurons. Second, we find that multiple classes of transcriptionally-conserved olfactory-bulb bound precursors are redirected to expanded primate white matter and striatum, including a novel peristriatal class, striatum laureatum neurons, that resemble dopaminergic periglomerular cells of the olfactory bulb. We propose an evolutionary model in which conserved initial classes of neurons supplying the smaller primate olfactory bulb are reused in the enlarged striatum and cortex. Together, our results provide a unified developmental taxonomy of initial classes of mammalian inhibitory neurons and reveal multiple developmental mechanisms for neural cell type evolution.
2021-11-23 | GSE169122 | GEO
Project description:Mutations in the solute carrier family 6-member 8 (Slc6a8) gene, encoding the protein responsible for cellular creatine (Cr) uptake, cause Creatine Transporter Deficiency (CTD), an X-linked neurometabolic disorder presenting with intellectual disability, autistic-like features, and epilepsy. The pathological determinants of CTD are still poorly understood, hindering the development of therapies. In this study, we generated an extensive transcriptomic profile of CTD showing that Cr deficiency causes perturbations of gene expression in excitatory neurons, inhibitory cells, and oligodendrocytes which result in remodeling of circuit excitability and synaptic wiring. We also identified specific alterations of parvalbumin-expressing (PV+) interneurons, exhibiting a reduction in cellular and synaptic density, and a hypofunctional electrophysiological phenotype. Mice lacking Slc6a8 only in PV+ interneurons recapitulated numerous CTD features, including cognitive deterioration, impaired cortical processing and hyperexcitability of brain circuits, demonstrating that Cr deficit in PV+ interneurons is sufficient to determine the neurological phenotype of CTD. Moreover, a pharmacological treatment targeted to restore the efficiency of PV+ synapses significantly improved cortical activity in Slc6a8 knock-out animals. Altogether, these data demonstrate that Slc6a8 is critical for the normal function of PV+ interneurons and that impairment of these cells is central in the disease pathogenesis, suggesting a novel therapeutic venue for CTD.
2023-03-14 | GSE216766 | GEO