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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE200569 | GEO | 2022/04/14

REPOSITORIES: GEO

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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

The long noncoding RNA neuroLNC modulates neurotransmitter release interacting with a neurodegeneration-associated protein

Project description:The roles of long noncoding RNAs (lncRNAs) in synaptic transmission and neuronal development are emerging. Here we applied an integrated bioinformatic/biological screening strategy to identify lncRNAs that regulate synaptic vesicle release. We identified neuroLNC, a conserved neuron-specific nuclear lncRNA that modulates synaptic vesicle release, presynaptic calcium influx, neurite elongation and neuronal migration. In neurons neuroLNC interacts with a neurodegeneration-associated protein and tunes a set of presynaptic transcripts implicated in neurotransmitter release.

2020-05-26 | PXD013434 | Pride

Microglial-derived C1q integrates into neuronal ribonucleoprotein complexes and impacts protein homeostasis in the aging brain

Project description:Neuroimmune interactions mediate intercellular communication and underlie critical brain functions. Microglia, CNS-resident macrophages, modulate the brain through direct physical interactions and the secretion of molecules. One such secreted factor, the complement protein C1q, contributes to complement-mediated synapse elimination in development and disease models, yet brain C1q protein levels increase significantly throughout aging. How age-related C1q affects neuronal function has not been demonstrated. Here we report that C1q interacts with neuronal ribonucleoprotein (RNP) complexes in an age-dependent manner. Purified C1q protein undergoes RNA-dependent liquid-liquid phase separation (LLPS) in vitro, and the interaction of C1q with neuronal RNP complexes in vivo is dependent on RNA and endocytosis. Mice lacking C1q have age-specific alterations in neuronal protein synthesis in vivo and impaired fear memory extinction. Together, our findings reveal a biophysical property of C1q that underlies RNA- and age-dependent neuronal interactions and demonstrate a unique role of C1q in critical intracellular neuronal processes.

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Interleukin-4 receptor signaling modulates neuronal network activity

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

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Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

Project description:Injury of descending motor tracts remodels cortical circuitry and leads to enhanced neuronal excitability, thus influencing recovery following injury. The neuron-specific contributions remain unclear due to the complex cellular composition and connectivity of the CNS. We developed a microfluidics-based in vitro model system to examine intrinsic synaptic remodeling following axon damage. We found that distal axotomy of cultured rat pyramidal neurons caused dendritic spine loss at synapses onto the injured neurons followed by a persistent retrograde enhancement in presynaptic excitability over days. These in vitro results mirrored hyper-activity of directly injured corticospinal neurons in hindlimb motor cortex layer Vb following spinal cord contusion. In vitro axotomy-induced hyper-excitability coincided with elimination of inhibitory presynaptic terminals, including those formed onto dendritic spines. We identified netrin-1 as downregulated following axotomy and exogenous netrin-1 applied 2 days after injury normalized spine density, presynaptic excitability, and the fraction of inhibitory inputs onto injured neurons. These findings demonstrate a novel model system for studying the response of pyramidal circuitry to axotomy and provide new insights of neuron-specific mechanisms that contribute to synaptic remodeling.

2016-11-02 | GSE89407 | GEO

Microglial-derived C1q integrates into neuronal ribonucleoprotein complexes and impacts protein homeostasis in the aging brain

Project description:Neuroimmune interactions mediate intercellular communication and underlie critical brain functions. Microglia, CNS-resident macrophages, modulate the brain through direct physical interactions and the secretion of molecules. One such secreted factor, the complement protein C1q, contributes to complement-mediated synapse elimination in development and disease models, yet brain C1q protein levels increase significantly throughout aging. Here we report that C1q interacts with neuronal ribonucleoprotein (RNP) complexes in an age-dependent manner. Purified C1q protein undergoes RNA-dependent liquid-liquid phase separation (LLPS) in vitro, and the interaction of C1q with neuronal RNP complexes in vivo is dependent on RNA and endocytosis. Mice lacking C1q have age-specific alterations in neuronal protein synthesis in vivo and impaired fear memory extinction. Together, our findings reveal a biophysical property of C1q that underlies RNA- and age-dependent neuronal interactions and demonstrate a role of C1q in critical intracellular neuronal processes.

2024-05-21 | MSV000094818 | MassIVE

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

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

| PRJNA825385 | ENA

Coordinated regulation of neuronal mRNA steady-state levels through developmentally controlled intron retention

Project description:Differentiated cells acquire unique structural and functional traits through coordinated expression of lineage-specific genes. An extensive battery of genes encoding components of the synaptic transmission machinery and specialized cytoskeletal proteins is activated during neurogenesis, but the underlying regulation is not well understood. Here we show that genes encoding critical presynaptic proteins are transcribed at a detectable level in both neurons and non-neuronal cells. However, in non-neuronal cells, the splicing of 3M-bM-^@M-^Y-terminal introns within these genes is repressed by polypyrimidine tract-binding protein (Ptbp1). This inhibits the export of incompletely spliced mRNAs to the cytoplasm and triggers their nuclear degradation. Clearance of these intron-containing transcripts occurs independently of the nonsense-mediated decay (NMD) pathway but requires components of the nuclear RNA surveillance machinery including the nuclear pore-associated protein Tpr and components of the exosome complex. When Ptbp1 expression decreases during neuronal differentiation, the regulated introns are spliced out thus allowing the accumulation of translation-competent mRNAs in the cytoplasm. We propose that this mechanism counters ectopic and precocious expression of functionally linked neuron-specific genes and ensures their coherent activation in the appropriate developmental context. PTBP1 siRNA, PTBP1+PTBP2 siRNA, or control siRNA

2012-07-12 | E-GEOD-37933 | biostudies-arrayexpress

Cortical bulk RNA sequencing of the microglia specific TREM2 inducible mouse models

Project description:We performed brain bulk RNA-seq aiming to study how microglia TREM2-WT or TREM2-R47H expression affect the overall brain transcriptomic profiles. Using WGCNA gene network analysis, we found the presynaptic transmission pathway was dysregulated after TREM2-R47H expression, not TREM2-WT. This finding was consistent with the impaired presynaptic transmission detected by electrophysiological recording in TREM2-R47H expressing mice. In addition, dysregulated circadian pathways were also identified in TREM2-R47H mice, not in TREM2-WT mice. Altogether, our bulk RNA-seq results provide additional evidence at transcriptomics level that TREM2-R47H expression in microglia affects neuronal functions and brain networks.

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A Specific Neuroligin3-αNeurexin1Signaling Regulates GABAergic Synaptic Function in Mouse Hippocampus

Project description:Synapses are fundamental organizers of precise signal propagation between neurons. Maintaining synapse assemblies require interactions between pre- and post- synaptic proteins, notably cell adhesion molecules (CAMs). It has been proposed that the function of Neuroligins (Nlgn1 - 4), postsynaptic CAMs, relies on the formation of trans-synaptic complexes with Neurexins (Nrxs), presynaptic CAMs. Nlgn3 is a unique Nlgn isoform that localizes at both excitatory and inhibitory synapses. However, Nlgn3 function mediated through Nrx interaction is mostly unknown. Here, we find for the first time that Nlgn3 localizes at postsynaptic sites apposing vesicular glutamate transporter 3 (VGT3)-expressing inhibitory terminals. Overexpression and knockdown approaches indicate that Nlgn3 regulates VGT3-positive inhibitory interneuron-mediated synaptic transmission. Fluorescent in situ hybridization and single-cell RNA sequencing studies revealed that αNrxn1 and βNrxn3 are VGT3 interneuron-specific Nrxn isoforms and the expression levels of Nrxn splice isoforms are highly diverse in VGT3 interneurons, respectively. Most importantly, postsynaptic Nlgn3 requires presynaptic αNrx1+AS4 expressed in VGT3-positive interneurons to regulate inhibitory synaptic transmission. Our results strongly suggest that specific Nlgn-Nrx interaction generate distinct functional properties at synapses.

2021-01-04 | GSE150989 | GEO

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