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RNA Sequencing quantitatively profiles chemical long-term potentiation (LTP) induced gene transcription alteration

ABSTRACT: To identify proteins involved in activity dependent synaptic remodeling that are not caused by changes in mRNA levels we performed RNA-seq and TMT-based quantitative MS.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE110908 | GEO | 2021/02/20

REPOSITORIES: GEO

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RNA Sequencing quantitatively profiles chemical long-term potentiation (LTP) induced gene transcription alteration

Project description:RNA Sequencing quantitatively profiles chemical long-term potentiation (LTP) induced gene transcription alteration

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Activity-Dependent Regulation of Alternative Cleavage and Polyadenylation (APA) during hippocampal Long-Term Potentiation (LTP) [3'READS]

Project description:This study was aimed at elucidating the mechanisms underlying activity-dependent gene regulation during LTP of mouse hippocampal CA3-CA1 synapses. Deep sequencing of the 3’ end of transcripts allowed to identify changes in APA induced 1 hour and 3 hours after LTP induction. We detected APA changes that only affected the 3'UTR (3'UTR-APA events) and APA changes that also affected the coding sequence (CDS-APA events).

2018-02-22 | GSE84643 | GEO

Activity-Dependent Regulation of Alternative Cleavage and Polyadenylation (APA) During Hippocampal Long-Term Potentiation (LTP) [RNA-Seq]

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Multiomics analysis of canine myocardium after circumferential pulmonary vein ablation: Effect of NPY on long-term reinduction of atrial fibrillation

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Stochastic Induction of Long-Term Potentiation and Long-Term Depression.

Project description:Long-term depression (LTD) and long-term potentiation (LTP) of granule-Purkinje cell synapses are persistent synaptic alterations induced by high and low rises of the intracellular calcium ion concentration ([Ca(2+)]), respectively. The occurrence of LTD involves the activation of a positive feedback loop formed by protein kinase C, phospholipase A2, and the extracellular signal-regulated protein kinase pathway, and its expression comprises the reduction of the population of synaptic AMPA receptors. Recently, a stochastic computational model of these signalling processes demonstrated that, in single synapses, LTD is probabilistic and bistable. Here, we expanded this model to simulate LTP, which requires protein phosphatases and the increase in the population of synaptic AMPA receptors. Our results indicated that, in single synapses, while LTD is bistable, LTP is gradual. Ca(2+) induced both processes stochastically. The magnitudes of the Ca(2+) signals and the states of the signalling network regulated the likelihood of LTP and LTD and defined dynamic macroscopic Ca(2+) thresholds for the synaptic modifications in populations of synapses according to an inverse Bienenstock, Cooper and Munro (BCM) rule or a sigmoidal function. In conclusion, our model presents a unifying mechanism that explains the macroscopic properties of LTP and LTD from their dynamics in single synapses.

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Mapping Gene Expression in Excitatory Neurons During Hippocampal Late-Phase Long-term Potentiation

Project description:The long-lasting changes in synaptic connectivity that underlie long-term memory require new RNA and protein synthesis for their persistence. To elucidate the temporal pattern of gene expression that gives rise to long-lasting, learning-related neuronal plasticity, we profiled RNAs in mouse hippocampal CA3-CA1 slices following induction of late phase long-term potentiation (LTP), analyzing differential expression (DE) specifically within pyramidal excitatory neurons by Translating Ribosome Affinity Purification RNA sequencing (TRAP-seq). We detected time-dependent changes in up- and down-regulated ribosome-associated mRNAs over the two hours following LTP induction, with minimal overlap of DE transcripts between time points. TRAP-seq revealed greater numbers and amplitudes of LTP-induced changes than RNA-seq of all cell types in the hippocampus. Transcripts that were DE by TRAP-seq but not RNA-seq were enriched in mRNAs encoding cytoskeletal and cell adhesion proteins, while RNA-seq identified DE in many non-neuronal mRNAs. Together our results highlight the importance of considering both the time course and the cell-type specificity of activity-dependent gene expression during memory formation.

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Proteasome and Autophagy-Mediated Impairment of Late Long-Term Potentiation (l-LTP) after Traumatic Brain Injury in the Somatosensory Cortex of Mice.

Project description:Traumatic brain injury (TBI) can lead to impaired cognition and memory consolidation. The acute phase (24-48 h) after TBI is often characterized by neural dysfunction in the vicinity of the lesion, but also in remote areas like the contralateral hemisphere. Protein homeostasis is crucial for synaptic long-term plasticity including the protein degradation systems, proteasome and autophagy. Still, little is known about the acute effects of TBI on synaptic long-term plasticity and protein degradation. Thus, we investigated TBI in a controlled cortical impact (CCI) model in the motor and somatosensory cortex of mice ex vivo-in vitro. Late long-term potentiation (l-LTP) was induced by theta-burst stimulation in acute brain slices after survival times of 1-2 days. Protein levels for the plasticity related protein calcium/calmodulin-dependent protein kinase II (CaMKII) was quantified by Western blots, and the protein degradation activity by enzymatical assays. We observed missing maintenance of l-LTP in the ipsilateral hemisphere, however not in the contralateral hemisphere after TBI. Protein levels of CaMKII were not changed but, interestingly, the protein degradation revealed bidirectional changes with a reduced proteasome activity and an increased autophagic flux in the ipsilateral hemisphere. Finally, LTP recordings in the presence of pharmacologically modified protein degradation systems also led to an impaired synaptic plasticity: bath-applied MG132, a proteasome inhibitor, or rapamycin, an activator of autophagy, both administered during theta burst stimulation, blocked the induction of LTP. These data indicate that alterations in protein degradation pathways likely contribute to cognitive deficits in the acute phase after TBI, which could be interesting for future approaches towards neuroprotective treatments early after traumatic brain injury.

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Development of a platform to investigate long term potentiation in human iPSC-derived neuronal networks

Project description:Although impairment of long-term potentiation (LTP) is a common feature of many neurological disorders, studies in humans are limited by inaccessibility of the brain. Human induced pluripotent stem cells (hiPSC) provide a unique opportunity to study LTP, especially in disease specific genetic backgrounds. We describe a multi-electrode array (MEA)-based assay to investigate chemically induced LTP (cLTP) in networks of hiPSC-derived midbrain dopaminergic (DA) and cortical neuronal populations. We demonstrate potentiation of activity that lasts for days, allowing for studies of the late phases of LTP. We show that cLTP on midbrain DA neuronal networks is largely independent of the N-methyl-D-aspartate receptor (NMDAR), and demonstrate partial dependence on brain derived neurotrophic factor (BDNF), as well as other factors released into the medium. Finally, we describe activity-regulated gene expression induced by cLTP. In summary, this cLTP-MEA assay platform will enable phenotype discovery and higher throughput analyses of synaptic plasticity on hiPSC-derived neurons.

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DNA-methylation of LTP-associated genes.

Project description:Long-term potentiation (LTP) of synaptic transmission is recognized as a cellular mechanism for learning and memory storage. Although de novo gene transcription is known to be required in the formation of stable LTP, the molecular mechanisms underlying synaptic plasticity remain elusive.This study investigates the DNA-methylation levels of promoters and CpG-islands of LTP-associated genes identified from Maag et al. 2015 (DOI: 10.3389/fnins.2015.00351) (See E-MTAB-3375).

2017-03-16 | E-MTAB-4919 | biostudies-arrayexpress

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