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

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

PROVIDER: PRJNA944932 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24299800.fastq.gz	Fastqsanger.gz
	SRR24299801.fastq.gz	Fastqsanger.gz
	SRR24299802.fastq.gz	Fastqsanger.gz
	SRR24299803.fastq.gz	Fastqsanger.gz
	SRR24299804.fastq.gz	Fastqsanger.gz

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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 (ChIP-Seq)

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, here we analyze the cellular and circuit functions of the genomic mechanisms that control the experience-induced transcription of Igf1 (Insulin-like growth factor 1) in VIP interneurons (INs) in the adult visual cortex. 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), and that 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 | GSE210656 | GEO

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

2023-06-27 | GSE227382 | GEO

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

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

| PRJNA866556 | ENA

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

Project description:Experience-dependent plasticity of synapses modulates information processing in neural circuits and is essential for cognitive functions. Genomic enhancers are thought to modulate specific sets of synapses by regulating experience-induced transcription to thereby promote neural circuit plasticity. However, this idea remains untested. Thus, here we analyze the cellular and circuit functions of the genomic mechanisms that control the experience-induced transcription of Igf1 (Insulin-like growth factor 1) in disinhibitory VIP interneurons in the adult visual cortex. We find that two sensory-induced enhancers selectively and cooperatively drive sensory-induced Igf1 transcription and that these enhancers homeostatically control the ratio between excitation and inhibition (E/I-ratio) and neural activity in VIP interneurons to thereby restrict visual acuity. Thus, single experience-regulated enhancers are essential for maintaining sensory processing. Since cortical plasticity scales with neural activity in VIP interneurons, this also suggests that experience-induced transcription restricts plasticity in adult neural circuits to preserve the brain’s functional integrity.

2023-06-27 | GSE227342 | GEO

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

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

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

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

| PRJNA944684 | ENA

Sensory experience remodels genome architecture in neural circuit to drive motor learning

Project description:Neuronal activity-dependent transcription couples sensory experience to adaptive responses of the brain including learning and memory. Mechanisms of activity-dependent gene expression including alterations of the epigenome have been characterized. However, the fundamental question of whether and how sensory experience remodels chromatin architecture in the adult brain in vivo to induce neural code transformations and learning and memory remains to be addressed. Here, in vivo calcium imaging, optogenetics, and pharmacological approaches reveal that granule neuron activation in the anterior dorsal cerebellar vermis (ADCV) plays a crucial role in a novel delay tactile startle learning paradigm in mice. Strikingly, using large-scale transcriptome and chromatin profiling, we have discovered that activation of the motor learning-linked granule neuron circuit reorganizes neuronal chromatin including through long-distance enhancer-promoter and transcriptionally active compartment interactions to orchestrate distinct granule neuron gene expression modules. Conditional CRISPR knockout of the chromatin architecture regulator Cohesin in ADCV granule neurons in adult mice disrupts activity-dependent transcription and motor learning. These findings define how sensory experience patterns chromatin architecture and neural circuit coding in the brain to drive motor learning.

2019-05-09 | GSE127995 | GEO

Sensory experience restricts cortical plasticity by inducing IGF-1 in VIP neurons

Project description:RNA-seq libraries purified from the visual cortices of neurons expressing Emx-, GAD2-, PV-, SST-, or VIP-Cre using the Ribotag allele. Seq libraries are provided from mice raised in standard housing, or housed in the dark for two weeks (dark-housed), or dark-housed and then exposed to light for 1, 3, or 7.5 hours. These seq libraries represent the genetic response of distinct types of cortical interneurons to altered sensory experience. To explore how sensory experience affects gene expression, we examined this process in the visual cortex of adult mice that were housed in standard conditions, in complete darkness (i.e. dark-housed), or dark-housed and then exposed to light for increasing amounts of time. We generated mice that were heterozygous for alleles of either Emx-,Gad2-,Sst-,Vip- or Pv-Cre, and were also heterozygous for the Rpl22-HA (RiboTag) allele, which expresses an HA-tagged ribosomal protein specifically in Cre-expressing neurons. We performed RNA-Seq on RNA isolated from the dark-housed/light-exposed RiboTag-mice; Experiments were done in 3 biological replicates and the visual cortices of 3 mice were pooled per sample at each time-point and for each Cre line.

2016-03-17 | E-GEOD-77243 | biostudies-arrayexpress

Proteomic landscape of the primary somatosensory cortex upon sensory deprivation

Project description:We employed label free quantitative mass spectrometry to address experience-dependent changes in the proteome after sensory deprivation in the primary somatosensory cortex. Cortical column- and layer-specific tissue samples were collected from control animals, with all whiskers intact, and animals whose C-row whiskers were bilaterally plucked for 11-14 days.

2017-08-24 | PXD005971 | Pride

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