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Development of specialized sensory neurons engages a nuclear receptor required for functional plasticity

ABSTRACT: Development of specialized sensory neurons engages a nuclear receptor required for functional plasticity

PROVIDER: PRJNA680300 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13111100_1.fastq.gz	Fastqsanger.gz
	SRR13111100_2.fastq.gz	Fastqsanger.gz
	SRR13111101_1.fastq.gz	Fastqsanger.gz
	SRR13111101_2.fastq.gz	Fastqsanger.gz
	SRR13111102_1.fastq.gz	Fastqsanger.gz

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Development of specialized sensory neurons engages a nuclear receptor required for functional plasticity.

Project description:During development, the nervous system generates neurons that serve highly specialized roles and, accordingly, possess unique functional attributes. The chemosensory BAG neurons of C. elegans are striking exemplars of this. BAGs sense the respiratory gas carbon dioxide (CO2) and, in a context-dependent manner, switch from mediating avoidance of CO2 to supporting CO2 attraction. To determine mechanisms that support the physiology and plasticity of BAG neurons, we used tandem ChIP-seq and cell targeted RNA-seq to identify gene targets of the transcription factor ETS-5, which is required for BAG development. A functional screen of ETS-5 targets revealed that NHR-6, the sole C. elegans NR4A-type nuclear receptor, is required for BAG-mediated avoidance of CO2 and regulates expression of a subset of BAG-specific genes. Unlike ets-5 mutants, which are defective for both attraction to and avoidance of CO2, nhr-6 mutants are fully competent for attraction. These data indicate that the remarkable ability of BAGs to adaptively assign positive or negative valence to a chemosensory stimulus requires a gene-regulatory program supported by an evolutionarily conserved type of nuclear receptor. We suggest that NHR-6 might be an example of a developmental mechanism for modular encoding of functional plasticity in the nervous system.

| S-EPMC7706712 | biostudies-literature

Development of specialized sensory neurons engages a nuclear receptor required for functional plasticity

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-23 | GSE162002 | GEO

Nutrigenomic regulation of sensory plasticity

Project description:Nutrigenomic regulation of sensory plasticity

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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

A nutriepigenetic pathway links diet to sensory plasticity

Project description:A nutriepigenetic pathway links diet to sensory plasticity

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Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

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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: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

Sensory system plasticity in a visually specialized, nocturnal spider.

Project description:The interplay between an animal's environmental niche and its behavior can influence the evolutionary form and function of its sensory systems. While intraspecific variation in sensory systems has been documented across distant taxa, fewer studies have investigated how changes in behavior might relate to plasticity in sensory systems across developmental time. To investigate the relationships among behavior, peripheral sensory structures, and central processing regions in the brain, we take advantage of a dramatic within-species shift of behavior in a nocturnal, net-casting spider (Deinopis spinosa), where males cease visually-mediated foraging upon maturation. We compared eye diameters and brain region volumes across sex and life stage, the latter through micro-computed X-ray tomography. We show that mature males possess altered peripheral visual morphology when compared to their juvenile counterparts, as well as juvenile and mature females. Matching peripheral sensory structure modifications, we uncovered differences in relative investment in both lower-order and higher-order processing regions in the brain responsible for visual processing. Our study provides evidence for sensory system plasticity when individuals dramatically change behavior across life stages, uncovering new avenues of inquiry focusing on altered reliance of specific sensory information when entering a new behavioral niche.

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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

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