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Transcriptional profile of migrating GABAergic progentitors in the E14 mouse brain following maternal exposure to cypermethrin and restraint stress

ABSTRACT: The goal of this experiment was to assess transcriptional changes in isolated GABAergic progenitors to determine the mechanism by which prenatal exposure to cypermethrin and maternal stress alter their migration

ORGANISM(S): Mus musculus

PROVIDER: GSE144511 | GEO | 2020/01/30

REPOSITORIES: GEO

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Transcriptional profile of migrating GABAergic progentitors in the E14 mouse brain following maternal exposure to cypermethrin and restraint stress

Project description:Transcriptional profile of migrating GABAergic progentitors in the E14 mouse brain following maternal exposure to cypermethrin and restraint stress

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Transcriptomic effects of prenatal exposure to corticosteroids on synaptic transmission

Project description:Prenatal exposure to synthetic corticosteroids can significantly alter postnatal development through changes in neurotransmitters and their receptors, and thus having long-lasting behavioral effects. Some of these changes have been observed in animal experiments, others also in humans prenatally exposed to synthetic corticosteroids. Here, we focused on transcriptomic changes within the prefrontal cortex of female rats prenatally exposed to either betamethasone or saline. The transcriptome has been assessed by novel computational tools to determine complex changes that may have life-long effects on phenotype, i.e., behavior. We analyzed how composition, topology and modulatory networks of the genomic fabric of the dopaminergic, GABAergic, and glutamatergic synapse (the transcriptome of the most interconnected and stably expressed gene network responsible for specific transmission) are afected by the prenatal exposure to corticosteroids and postnatal ketamine-induced seizures. One sex (F) x two prenatal exposures (B = betamethasone, S = saline) x two postnatal treatments (K = ketamine, S = saline). Biological replicates: 4 FSS, 4 FBS, 4 FBK.

2016-01-09 | E-GEOD-76694 | biostudies-arrayexpress

Rapid conversion of fibroblasts into functional forebrain GABAergic interneurons by direct genetic reprogramming

Project description:Transplantation of GABAergic interneurons (INs) can sustain long-standing benefits in animal models of epilepsy and other neurological disorders. In a therapeutic perspective, a renewable source of functional GABAergic INs is needed. Here, we identified five factors (Foxg1, Sox2, Ascl1, Dlx5 and Lhx6) able to convert fibroblasts directly into induced GABAergic INs (iGABA-INs), displaying the molecular signature of telencephalic INs. The selected factors recapitulate in fibroblasts the activation of transcriptional networks required for the specification of GABAergic fate during telencephalon development. iGABA-INs exhibited progressively maturing firing patterns comparable to those of cortical INs, had synaptic currents and released GABA. Importantly, upon grafting in the hippocampus, iGABA-INs survived, matured and their optogenetic stimulation triggered GABAergic transmission and inhibited the activity of connected granule cells. The five factors also converted human cells into functional GABAergic neurons. These properties define iGABA-INs as a promising tool for disease modeling and cell-based therapeutic approaches. Comparison of iGABA-INs transcriptional profile with those of starting fibroblasts and GAD67-GFP+ cortical interneurons.

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Four GABAergic interneurons impose feeding restraint in Drosophila.

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Expression profiling in cortical GABAergic neurons at neonate

Project description:During embryonic development, GABAergic interneurons, a main inhibitory component in the cerebral cortex, migrate tangentially from the ganglionic eminence (GE) to cerebral cortex. After reaching the cerebral cortex, they start to extend their neurites for constructing local neuronal circuits around the neonatal stage. Aberrations in migration or neurite outgrowth are implicated in neurological and psychiatric disorders such as epilepsy, schizophrenia and autism. Previous studies revealed that in the early phase of cortical development the neural population migrates tangentially from the GE in the telencephalon and several genes have been characterized as regulators of migration and specification of GABAergic interneurons. However, much less is known about the molecular mechanisms of GABAergic interneurons-specific maturation at later stages of development. Here, we performed genome-wide screening to identify genes related to the later stage by flow cytometry based-microarray (FACS-array) and identified 247 genes expressed in cortical GABAergic interneurons. Among them, Dgkg, a member of diacylglycerol kinase family, was further analyzed. Correlational analysis revealed that Dgkg is dominantly expressed in somatostatin (SST)-expressing GABAergic interneurons. The functional study of Dgkg using GE neurons indicated alteration in neurite outgrowth of GABAergic neurons. This study shows a new functional role for Dgkg in GABAergic interneurons as well as the identification of other candidate genes for their maturation.

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Gene expression profiles of intermediate progenitors of GABAergic neuron

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Project description:How neurons are wired to form precise circuits is crucial to understand the development of cortical functions. Glutamatergic pyramidal cell and GABAergic interneuron wire up the cortex through differentiated cellular events. However, little is known about the molecular mechanisms that underlie the unique features of interneuron wiring. We performed a high-throughput genomic screen for genes upregulated specifically during GABAergic wiring.

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Asymmetric dynamics of GABAergic system and paradoxical responses of GABAergic neurons in piriform seizures

Project description:Asymmetric dynamics of GABAergic system and paradoxical responses of GABAergic neurons in piriform seizures

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Asymmetric dynamics of GABAergic system and paradoxical responses of GABAergic neurons in piriform seizures

Project description:The piriform cortex (PC) plays a critical role in epileptogenesis, where an excitation/inhibition imbalance contributes to epilepsy etiology. However, the epileptic dynamics of the GABA system and the precise role of GABAergic neurons within the PC in epilepsy remain unclear. Here, we combined Ca2+ and GABA sensors to investigate the dynamics of Gad2-expressing neurons and GABA levels, and selectively manipulated GABAergic neurons in the PC through chemogenetic inhibition and caspase3-mediated apoptosis targeting Gad2 interneurons. The chronic deficiency of PC Gad2 neurons triggered spontaneous recurrent seizures. These findings uncover the dynamic interplay within PC inhibitory components and elaborate counteractive mechanisms in seizure regulation.

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