Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Training-induced excitatory synaptogenesis in a prefrontal cortex circuit is required for effort/reward evaluation

ABSTRACT: Training-induced excitatory synaptogenesis in a prefrontal cortex circuit is required for effort/reward evaluation

PROVIDER: PRJNA716510 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14041311_1.fastq.gz	Fastqsanger.gz
	SRR14041311_2.fastq.gz	Fastqsanger.gz
	SRR14041312_1.fastq.gz	Fastqsanger.gz
	SRR14041312_2.fastq.gz	Fastqsanger.gz
	SRR14041313_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

Training-induced excitatory synaptogenesis in a prefrontal cortex circuit is required for effort/reward evaluation

Project description:We report bulk RNAseq data obtained from the Anterior Cingulate Cortex (ACC) microdissected from Untrained (n=5) and Trained (n=6) wild-type mice for an instrumental task, the lever-press task for food reward.

2021-03-24 | GSE169392 | GEO

Astrocyte-derived thrombospondins 1 and 2 are required for cortical synapse development controlling goal-directed action performance.

Project description:During development, controlled synaptogenesis is required to form functioning neural circuits that underlie cognition and behavior. Astrocytes, a major glial-cell type in the central nervous system (CNS), promote synapse formation by secreting synaptogenic proteins. Thrombospondins 1 and 2 (TSP1/2), which act through their neuronal receptor α2δ-1, are required for proper intracortical excitatory synaptogenesis. In the adult brain, the loss of α2δ-1 impairs training-induced excitatory synaptogenesis in the anterior cingulate cortex (ACC), and this impairment leads to increased effort-exertion during high-effort tasks. Here, we tested whether TSP1 and TSP2 are required for controlling effort during operant conditioning by using a lever press for food reward training in mice. Surprisingly, we found that constitutive loss of TSP1/2 significantly reduced lever pressing performance when the effort required for a food reward was increased, a phenotype opposite of α2δ-1 loss. Loss of TSP1/2 reduced excitatory synapse number significantly in adult brains. However, in the ACC of TSP1/2 knockout mice, there was still training-induced excitatory synaptogenesis, likely through the upregulation of TSP4, a TSP isoform that is also synaptogenic. Unexpectedly, we also found a significant increase in inhibitory synapse number and function in the ACC of TSP1/2 knockout mice, which were eliminated after training. Finally, we found that astrocyte-specific ablation of TSP1/2 in developing but not adult astrocytes is sufficient to reduce performance during high-effort tasks. Taken together, our study highlights the importance of developmental astrocyte-derived synaptogenic cues TSP1 and 2 in establishing excitatory and inhibitory circuits that control effort during operant conditioning in adults.

2024-02-29 | GSE257869 | GEO

A human-specific microRNA controls the timing of excitatory synaptogenesis

Project description:A human-specific microRNA controls the timing of excitatory synaptogenesis

| PRJNA1023169 | ENA

Training-induced circuit-specific excitatory synaptogenesis in mice is required for effort control.

Project description:Synaptogenesis is essential for circuit development; however, it is unknown whether it is critical for the establishment and performance of goal-directed voluntary behaviors. Here, we show that operant conditioning via lever-press for food reward training in mice induces excitatory synapse formation onto a subset of anterior cingulate cortex neurons projecting to the dorsomedial striatum (ACC→DMS). Training-induced synaptogenesis is controlled by the Gabapentin/Thrombospondin receptor α2δ-1, which is an essential neuronal protein for proper intracortical excitatory synaptogenesis. Using germline and conditional knockout mice, we found that deletion of α2δ-1 in the adult ACC→DMS circuit diminishes training-induced excitatory synaptogenesis. Surprisingly, this manipulation does not impact learning but results in a significant increase in effort exertion without affecting sensitivity to reward value or changing contingencies. Bidirectional optogenetic manipulation of ACC→DMS neurons rescues or phenocopies the behaviors of the α2δ-1 cKO mice, highlighting the importance of synaptogenesis within this cortico-striatal circuit in regulating effort exertion.

| S-EPMC10491649 | biostudies-literature

A human-specific microRNA controls the timing of excitatory synaptogenesis

Project description:The development of neural circuits in the human cortex is considerably prolonged in comparison to non-human primates, a trait which contributes to the remarkable cognitive capacity of modern humans. In contrast to protein-coding genes, non-coding genes underwent a dramatic expansion during evolution, suggesting their involvement in human-specific aspects of brain development. Here, using a glial free human-induced pluripotent stem-cell derived neuron model (“igNeurons”), we show widespread expression and dynamic regulation of various non-coding RNA classes, including microRNAs, during human excitatory synapse development. The expression of a human-specific microRNA, miR-1229-3p, strongly correlates with the neuromorphological trajectory of igNeurons. miR-1229-3p inhibition promotes the formation of excitatory synaptic co-clusters at early stages but reduces dendritic arborization in more mature neurons, consistent with accelerated neuronal maturation. Morphological alterations are accompanied by enhanced calcium spike activity and excitatory synaptic transmission. Mechanistically, miR-1229-3p controls mitochondrial homeostasis by directly targeting important regulators of mitochondrial autophagy and fission, such as Pink1. Stimulation of mitochondrial metabolism rescues the enhanced calcium spike activity in miR-1229-3p depleted neurons, demonstrating a causal involvement of mitochondrial homeostasis. Thus, our findings reveal an important function of human-specific miR-1229-3p in developmental timing of human synaptogenesis and generally implicate non-coding RNAs in the control of human connectivity and cognition.

2025-11-03 | PXD045809 | Pride

A human-specific microRNA controls the timing of excitatory synaptogenesis (pLNA dataset)

Project description:A human-specific microRNA controls the timing of excitatory synaptogenesis (pLNA dataset)

| PRJNA1023177 | ENA

A human-specific microRNA controls the timing of excitatory synaptogenesis (time course smallRNA)

Project description:A human-specific microRNA controls the timing of excitatory synaptogenesis (time course smallRNA)

| PRJNA1023178 | ENA

A human-specific microRNA controls the timing of excitatory synaptogenesis (time course ribozero)

Project description:A human-specific microRNA controls the timing of excitatory synaptogenesis (time course ribozero)

| PRJNA1023176 | ENA

Neuronal activation modulates enhancer activity of genes for excitatory synaptogenesis through de novo DNA methylation

Project description:Post-mitotic neurons exhibit DNA methylation changes, contrary to the longstanding belief that the epigenetic pattern in terminally differentiated cells is essentially unchanging. While the mechanism and physiological significance of DNA demethylation in neurons have been extensively elucidated, occurrence of de novo DNA methylation and its impacts have been much less investigated. Here we show that neuronal activation induces global de novo DNA methylation at enhancer regions that can repress target genes in primary cultured hippocampal neurons. The functional significance of this de novo DNA methylation was underpinned by the demonstration that inhibition of DNA methyltransferase (DNMT) activity decreased neuronal activity-induced excitatory synaptogenesis. Overexpression of WW and C2 Domain containing 1 (Wwc1), a representative target gene of de novo DNA methylation, could phenocopy this DNMT inhibition-induced decrease in the synaptogenesis. We found that both DNMT1 and DNMT3a were required for the neuronal activity-induced de novo DNA methylation of Wwc1 enhancer. Taking these findings altogether, we concluded that activity-induced de novo DNA methylation affecting gene expression has impacts on neuronal physiology comparable to those of DNA demethylation.

2020-04-26 | GSE149342 | GEO

A human-specific microRNA controls the timing of excitatory synaptogenesis (pLNA dataset)

Project description:Neural circuit development in the human cortex is considerably prolonged in comparison to non-human primates, a trait that contributes to the remarkable cognitive capacity of modern humans. Here, we explore the regulatory role of non-coding RNAs, which dramatically expanded during brain evolution, in synapse development of human-induced pluripotent stem-cell derived neurons. We found that inhibition of a human-specific microRNA, miR-1229-3p, alters the trajectory of human neuronal maturation and enhances excitatory synaptic transmission. Transcriptome analysis following miR-1229 knockdown revealed a downregulation of mitochondrial DNA (mtDNA) encoded genes. We further show that miR-1229 regulates mitochondrial morphology, mtDNA abundance and matrix calcium concentration, and that stimulation of mitochondrial metabolism rescues decreased calcium buffering in miR-1229-3p depleted neurons. Accordingly, miR-1229 directly targets an entire network of genes involved in mitochondrial function and ER-associated protein homeostasis. Our findings reveal an important function of human-specific miR-1229-3p in developmental timing of human synaptogenesis and generally implicate non-coding RNAs in the control of human connectivity and cognition.

2025-10-30 | GSE244441 | 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