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A novel hippocampal long-range VIP-GABAergic projection to subiculum contributes to fear memory formation through region-specific connectivity

ABSTRACT: We sequenced seven long-range projection vasoactive intestinal peptide (VIP)-expressing interneurons from the mouse CA1 oriens/alveus area using patch-seq technique to determine their molecular identity.

ORGANISM(S): Mus musculus

PROVIDER: GSE109755 | GEO | 2018/01/30

REPOSITORIES: GEO

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A novel hippocampal long-range VIP-GABAergic projection to subiculum contributes to fear memory formation through region-specific connectivity

Project description:A novel hippocampal long-range VIP-GABAergic projection to subiculum contributes to fear memory formation through region-specific connectivity

| PRJNA431967 | ENA

Identification of the Early VIP Transriptome and its Associated Interactome in Activated Murine CD4 T Cells

Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Activated Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the presence of PMA/ionomycin (activated) for five hours with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. PMA/ionomycin (activated) mouse CD4 T spleenocytes with VIP ligand (sample) vs. PMA/ionomycin (activated) mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.

2010-01-09 | E-GEOD-18525 | biostudies-arrayexpress

Identification of the Early VIP Transriptome and its Associated Interactome in Resting Murine CD4 T Cells

Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Resting Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the absence of PMA/ionomycin (resting) with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. Naïve mouse CD4 T spleenocytes with VIP ligand (sample) vs. naïve mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.

2010-01-09 | E-GEOD-18524 | biostudies-arrayexpress

Identification of the Early VIP Transriptome and its Associated Interactome in Resting Murine CD4 T Cells

2010-01-09 | GSE18524 | GEO

DUSP4 regulates input to the suprachiasmatic circadian network via VIP-induced activation of the ERK1/2 pathway

Project description:Analysis of the genes and cellular signalling cascades mediating the response of SCN slices to vasoactive intestinal peptide (VIP). Primary goal was to find novel genes that may be involved in circadian phase shifting for further study. Promoter analysis of significantly regulated genes and gene ontology analysis would provide information into pathways VIP acts through in the SCN.

2019-02-07 | GSE113797 | GEO

Identification of the Early VIP Transriptome and its Associated Interactome in Activated Murine CD4 T Cells

2010-01-09 | GSE18525 | GEO

Cholangiocytic cysts (CCs) treated with or without vasoactive intestinal peptide (VIP)

Project description:Cholangiocytic cysts (CCs) treated with or without vasoactive intestinal peptide (VIP)

| PRJNA580026 | ENA

Single genomic enhancers drive experience-dependent GABAergic plasticity to maintain sensory processing in the adult cortex

Project description:Experience-dependent plasticity of synapses modulates information processing in neural circuits and is essential for cognitive functions. The genome, via non-coding enhancers, was proposed to control information processing and circuit plasticity by regulating experience-induced transcription of genes that modulate specific sets of synapses. To test this idea, we analyze here the cellular and circuit functions of the genomic mechanisms that control the experience-induced transcription of Igf1 (insulin-like growth factor 1) in vasoactive intestinal peptide (VIP) interneurons (INs) in the visual cortex of adult mice. We find that two sensory-induced enhancers selectively and cooperatively drive the activity-induced transcription of Igf1 to thereby promote GABAergic inputs onto VIP INs and to homeostatically control the ratio between excitation and inhibition (E/I ratio)—in turn, this restricts neural activity in VIP INs and principal excitatory neurons and maintains spatial frequency tuning. Thus, enhancer-mediated activity-induced transcription maintains sensory processing in the adult cortex via homeostatic modulation of E/I ratio.

2023-06-27 | GSE210658 | GEO

Single genomic enhancers drive experience-dependent GABAergic plasticity to maintain sensory processing in the adult cortex (RNA-Seq)

2023-06-27 | GSE227382 | GEO

HDAC3 Inhibition Causes the Impairment in Development of Neocortical VIP Interneurons via dysregulation of Notch Signaling and Autism-like Behaviors

Project description:Autism spectrum disorders (ASDs) are a neurodevelopmental disorder characterized by impairments in social interactions and stereotyped behaviors. While ASD has a strong genetic background, environmental factors including toxins, pesticides, infection and drugs are also known to confer autism susceptibility, likely by inducing epigenetic changes. Exposure to Valproic acid (VPA), a drug for epilepsy and bipolar disorders, during pregnancy is highly associated with the risk of ASD children. In rodents, in utero VPA exposure can precipitate behavioral phenotypes related to ASD in the offspring. Since VPA is an inhibitor of histone deacethytransferase (HDAC) activity, it thought to cause ASD with epigenetic modification. However, the core mechanism by which prenatal VPA exposure causes onset of ASD is still not fully uncovered. Here we revealed that prenatal VPA exposure strongly influences development of vasoactive intestinal peptide (VIP) - positive neurons, a subtype of cortical GABAergic interneurons. The number of VIP+ interneurons was severely reduced in somatosensory area of VPA-exposed ASD animals. We then found that the reduction in VIP+ interneurons is caused by the inhibition of HDAC3 activity upon prenatal VPA exposure. Importantly, prenatal HDAC3 inhibition caused not only the selective reduction in VIP+ interneurons but also the ASD-like behaviors in mice. We then demonstrated that the HDAC3 inhibition aberrantly activates Notch signaling, which influences the cell fate determination of VIP+ interneuron progenitors in caudal ganglionic eminence. Thus, this study uncovers the mechanism by which specific HDAC inhibition during development influences a specific type of GABAergic interneurons in the ASD model. The findings provide a novel insight into the understanding of ASD pathophysiology.

2022-06-20 | GSE133932 | GEO

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