Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Interleukin-4 receptor signaling modulates neuronal network activity [mouse]

ABSTRACT: Interleukin-4 receptor signaling modulates neuronal network activity [mouse]

PROVIDER: PRJNA825385 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18709073_1.fastq.gz	Fastqsanger.gz
	SRR18709073_2.fastq.gz	Fastqsanger.gz
	SRR18709074_1.fastq.gz	Fastqsanger.gz
	SRR18709074_2.fastq.gz	Fastqsanger.gz
	SRR18709075_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 13

Similar Datasets

Interleukin-4 receptor signaling modulates neuronal network activity

Project description:Interleukin-4 receptor signaling modulates neuronal network activity

| PRJNA825260 | ENA

Interleukin-4 receptor signaling modulates neuronal network activity

Project description:Neuroimmune interaction influences essential CNS processes. Hanuscheck et al. report expression of interleukin-4 receptor alpha at presynaptic terminals in mouse and human brain. Modulation of neuronal IL-R signaling alters the neuronal transcriptome, impacts synaptic transmission and causes anxiety-related behavior.

2022-04-13 | GSE200555 | GEO

Interleukin-4 receptor signaling modulates neuronal network activity [mouse]

2022-04-14 | GSE200569 | GEO

Interleukin-4 receptor signaling modulates neuronal network activity.

Project description:Evidence is emerging that immune responses not only play a part in the central nervous system (CNS) in diseases but may also be relevant for healthy conditions. We discovered a major role for the interleukin-4 (IL-4)/IL-4 receptor alpha (IL-4Rα) signaling pathway in synaptic processes, as indicated by transcriptome analysis in IL-4Rα-deficient mice and human neurons with/without IL-4 treatment. Moreover, IL-4Rα is expressed presynaptically, and locally available IL-4 regulates synaptic transmission. We found reduced synaptic vesicle pools, altered postsynaptic currents, and a higher excitatory drive in cortical networks of IL-4Rα-deficient neurons. Acute effects of IL-4 treatment on postsynaptic currents in wild-type neurons were mediated via PKCγ signaling release and led to increased inhibitory activity supporting the findings in IL-4Rα-deficient neurons. In fact, the deficiency of IL-4Rα resulted in increased network activity in vivo, accompanied by altered exploration and anxiety-related learning behavior; general learning and memory was unchanged. In conclusion, neuronal IL-4Rα and its presynaptic prevalence appear relevant for maintaining homeostasis of CNS synaptic function.

| S-EPMC9123307 | biostudies-literature

FMRP phosphorylation modulates neuronal translation through YTHDF1

Project description:FMRP phosphorylation modulates neuronal translation through YTHDF1

| PRJNA887460 | ENA

Nedd4-2-dependent regulation of astrocytic Kir4.1 and Connexin43 controls neuronal network activity

Project description:Nedd4-2 is an E3 ubiquitin ligase in which missense mutation is related to familial epilepsy, indicating its critical role in regulating neuronal network activity. However, Nedd4-2 substrates involved in neuronal network function have yet to be identified. Using mouse lines lacking Nedd4-1 and Nedd4-2 and an isobaric labeling approach for quantitative comparison of the synaptic membrane proteome, we identified astrocytic channel proteins inwardly rectifying potassium channel 4.1 (Kir4.1) and Connexin43 as upregulated in ubiquitin ligase knockout mice and thus as candidate Nedd4-2 substrates. Kir4.1 and Connexin43 were confirmed as Nedd4-2 substrates by independent methods and their functional role in astrocytes as to modulation of neuronal network activity was established.

2023-11-28 | PXD046450 | Pride

Serpina3 modulates neuronal cell fate determination (scRNA sequencing)

Project description:Serpina3 modulates neuronal cell fate determination (scRNA sequencing)

| PRJNA694621 | ENA

Lipid Accumulation Induced by APOE4 Impairs Microglial Surveillance of Neuronal-Network Activity

Project description:Apolipoprotein E4 (APOE4) is the greatest known genetic risk factor for developing late-onset Alzheimer’s disease and its expression in microglia is associated with pro-inflammatory states. How the interaction of APOE4 microglia with neurons differs from microglia expressing the disease-neutral allele APOE3 is currently unknown. Here, we employ CRISPR-edited induced pluripotent stem cells (iPSCs) to dissect the impact of APOE4 in neuron-microglia communication. Our results reveal that APOE4 induces a distinct metabolic program in microglia that is marked by the accumulation of intracellular neutral lipid stores through impaired lipid catabolism. Importantly, this altered lipid-accumulated state shifts microglia away from homeostatic surveillance and renders APOE4 microglia weakly responsive to neuronal activity. By examining the transcriptional signatures of APOE3 versus APOE4 microglia before and after exposure to neuronal conditioned media, we further established that neuronal soluble cues differentially induce a lipogenic program in APOE4 microglia that exacerbates pro-inflammatory signals. Pharmacological blockade of lipogenesis in APOE4 microglia is sufficient to diminish intracellular lipid accumulation and restore microglial homeostasis. Remarkably, unlike APOE3 microglia that support neuronal network activity, co-culture of APOE4 microglia with neurons disrupts the coordinated activity of neuronal ensembles. We identified that through decreased uptake of extracellular fatty acids and lipoproteins, APOE4 microglia disrupts the net flux of lipids which results in decreased neuronal activity via the potentiation of the lipid-gated K+ channel, GIRK3. These findings suggest that neurological diseases that exhibit abnormal neuronal network-level disturbances may in part be triggered by impairment in lipid homeostasis in non-neuronal cells, underscoring a novel therapeutic route to restore circuit function in the diseased brain.

2022-05-19 | GSE203019 | GEO

Hypomorphic ASGR1 Modulates Lipid Homeostasis via SREBPs Network

Project description:Hypomorphic ASGR1 Modulates Lipid Homeostasis via SREBPs Network

| PRJNA738702 | ENA

Aberrant Neuronal Connectivity and Network Activity of Neurons Derived from Patients with Idiopathic Schizophrenia

Project description:Schizophrenia (SCZ) is a psychiatric disorder with a strong genetic determinant. A major hypothesis to explain disease aetiology comprises synaptic dysfunction associated with excitatory-inhibitory imbalance of synaptic transmission, ultimately contributing to impaired network oscillation and cognitive deficits associated with the disease. Here, we studied the morphological and functional properties of a highly defined co-culture of GABAergic and glutamatergic neurons derived from induced pluripotent stem cells (iPSC) from patients with idiopathic SCZ. Our results indicate upregulation of synaptic genes and increased excitatory synapse formation on GABAergic neurons in co-cultures. In parallel, we observed decreased lengths of axon initial segments, concordant with data from postmortem brains from patients with SCZ. Patch-clamp analyses revealed differential processing of excitatory input with markedly increased spontaneous excitatory postsynaptic currents (EPSC) recorded from GABAergic SCZ neurons and decreased spontaneous EPSC from glutamatergic SCZ neurons. Likewise, we observed decreased amplitudes of calcium signals selectively in GABAergic neurons while frequency was increased in both neuronal populations. Finally, MEA recordings from neuronal networks indicate increased synchronization of network activity. In conclusion, our results suggest selective deregulation of neuronal activity and synaptic transmission in SCZ samples, providing evidence for differential signal processing in GABAergic and glutamatergic neurons as a potential base for aberrant network synchronization.

2024-11-25 | GSE282524 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data