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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE227342 | GEO | 2023/06/27

REPOSITORIES: GEO

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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

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

Mus musculus

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

| PRJNA309869 | ENA

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

2016-03-17 | GSE77243 | GEO

Merkel Cells Activate Sensory Neural Pathways through Adrenergic Synapses

Project description:Merkel Cells Activate Sensory Neural Pathways through Adrenergic Synapses

| PRJNA470987 | ENA

Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

Project description:The nervous system has a tremendous capacity for experience-dependent plasticity. In response to changes in activity induced by environmental cues, many types of neurons undergo a process known as homeostatic plasticity, which serves to maintain overall network function in the face of mounting experience-dependent changes in synaptic strengths. Homeostatic plasticity involves both changes in synaptic scaling and regulation of intrinsic excitability. Increases in spontaneous firing and excitability of sensory neurons are evident in some forms of chronic pain in both animal models and in human patients. However, it is not known whether homeostatic plasticity is engaged in sensory neurons under normal conditions or whether dysfunction in these homeostatic mechanisms might contribute to the pathophysiology of chronic pain. To address these questions, we tested the impact of sustained depolarization on various measures of excitability in mouse and human sensory neurons. Depolarization induced by 30mM KCl induces a compensatory decrease in the excitability of both mouse and human sensory neurons. Moreover, we also find that voltage-gated sodium currents are robustly inhibited in mouse sensory neurons after chronic depolarization, thus contributing to the overall decrease in neuronal excitability and serving as a potential regulatory mechanism to drive intrinsic neuronal homeostatic control. Our results indicate that mouse and human sensory neurons undergo homeostatic regulation of intrinsic excitability in response to sustained depolarization. Decreased efficacy of these homeostatic mechanisms could potentially contribute to the development of pathological conditions, including chronic pain.

2024-01-31 | GSE236109 | GEO

Experience-induced remodeling of the hippocampal post-synaptic proteome and phosphoproteome

Project description:The postsynaptic density (PSD) of excitatory synapses contains a highly organized protein network with thousands of proteins and is key node in the regulation of synaptic plasticity. To gain new mechanistic insight into experience-induced changes in the PSD, we examined the global dynamics of the hippocampal PSD proteome and phosphoproteome in mice following 4 different types of experience. Mice were trained using an inhibitory avoidance (IA) task and hippocampal PSD fractions were isolated from individual mice to investigate molecular mechanisms underlying experience-dependent remodeling of synapses. We developed a new strategy to identify and quantify the relatively low level of site-specific phosphorylation of PSD proteome from the hippocampus, by using a modified iTRAQ-based TiSH protocol. In the PSD, we identified 3,938 proteins and 2,761 phosphoproteins in the sequential strategy covering a total of 4,968 unique protein groups (at least 2 peptides including an unique peptide). On the phosphoproteins, we identified a total of 6,188 unambiguous phosphosites (75% site localization probability)

2024-01-26 | PXD045496 | Pride

Acute synthesis of CPEB is required for plasticity of visual avoidance behavior in Xenopus

Project description:Neural plasticity requires protein synthesis, but the identity of newly synthesized proteins generated in response to plasticity-inducing stimuli remains unclear. We used in vivo bio-orthogonal noncanonical amino acid tagging (BONCAT) with the methionine analog azidohomoalanine (AHA) combined with the multidimensional protein identification technique (MudPIT) to identify proteins that are synthesized in the tadpole brain over 24 hr. We induced conditioning-dependent plasticity of visual avoidance behavior, which required N-methyl-D-aspartate (NMDA) and Ca(2+)-permeable alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, alphaCaMKII, and rapid protein synthesis. Combining BONCAT with western blots revealed that proteins including alphaCaMKII, MEK1, CPEB, and GAD65 are synthesized during conditioning. Acute synthesis of CPEB during conditioning is required for behavioral plasticity as well as conditioning-induced synaptic and structural plasticity in the tectal circuit. We outline a signaling pathway that regulates protein-synthesis-dependent behavioral plasticity in intact animals, identify newly synthesized proteins induced by visual experience, and demonstrate a requirement for acute synthesis of CPEB in plasticity.

2018-01-11 | MSV000081914 | MassIVE

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