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Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected after acute swim stress

ABSTRACT: We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress.

ORGANISM(S): Mus musculus

PROVIDER: GSE47847 | GEO | 2014/07/01

SECONDARY ACCESSION(S): PRJNA208121

REPOSITORIES: GEO

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Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected at rest

2014-07-01 | GSE47846 | GEO

Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected after acute swim stress

Project description:We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naM-CM-/ve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest and after acute stress (this study).

2014-07-01 | E-GEOD-47847 | biostudies-arrayexpress

Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected at rest

2014-07-01 | E-GEOD-47846 | biostudies-arrayexpress

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

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

Project description:This study was aimed at elucidating the mechanisms underlying activity-dependent gene regulation during long-term potentiation (LTP) of mouse hippocampal CA3-CA1 synapses. Transcriptome analysis allowed to identify changes in gene expression and alternative splicing induced 1 hour and 3 hours after LTP induction.

2018-02-22 | GSE84503 | GEO

Smolen2018 - Paradoxical LTP maintenance with inhibition of protein synthesis and the proteasome

Project description:This is a mathematical model describing the formation of long-term potentiation (LTP) at the Schaffer collateral of CA1 pyramidal cell synapse. The model consists of nine ordinary differential equations that denote synaptic states associated with different degrees of LTP, as well as the levels of regulatory proteins involved in the formation and maintenance of LTP.

2024-09-02 | BIOMD0000000853 | BioModels

Li2019 - Neurogranin stimulates Ca/calmodulin-dependent kinase II by inhibiting Calcineurin

Project description:Calmodulin sits at the center of molecular mechanisms underlying learning and memory. Its complex, and sometimes opposite, influences via the binding to various proteins are yet to be fully understood. Calcium/calmodulin-dependent protein kinase II (CaMKII) and calcineurin (CaN) both bind open calmodulin, favoring Long-term-potentiation (LTP) or depression (LTD) respectively. Neurogranin binds to the closed conformation of calmodulin and its impact on synaptic plasticity is less clear. We set up a mechanistic computational model based on allosteric principles to simulate calmodulin state transitions and its interaction with calcium ions and the three binding partners mentioned above. We simulated calcium spikes at various frequencies and show that neurogranin regulates synaptic plasticity along three modalities. At low spike frequencies, neurogranin inhibits the onset of LTD by limiting CaN activation. At intermediate frequencies, neurogranin limits LTP by precluding binding of CaMKII with calmodulin. Finally, at high spike frequencies, neurogranin promotes LTP by enhancing CaMKII autophosphorylation. While neurogranin might act as a calmodulin buffer, it does not significantly preclude the calmodulin opening by calcium. On the contrary, neurogranin synchronizes the opening of calmodulin's two lobes and promotes their activation at specific frequencies, increasing the chance of CaMKII trans-autophosphorylation. Importantly, the positive effect of neurogranin on CaMKII activation is mediated via CaN, and too few or too much CaN will abolish this effect. Furthermore, the amount of neurogranin itself differentially regulates the levels of CaN and CaMKII activities, as well as the frequencies at which the balance switch from one to the other.

2019-12-18 | MODEL1903010001 | BioModels

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.

2022-08-18 | GSE193191 | GEO

Gene profiling of VP16-CREB transgenic mice

Project description:Expression of VP16-CREB, a constitutively active form of CREB, in hippocampal neurons of the CA1 region lowers the threshold for eliciting the late, persistent phase of long-term potentiation (L-LTP) in the Schaffer collateral pathway. This VP16-CREB-mediated L-LTP differs from the conventional late phase of LTP in not being dependent on new transcription. This finding suggests that in the transgenic mice the mRNA transcript(s) encoding the protein(s) necessary for this form of L-LTP might already be present in CA1 neurons in the basal condition. We used high-density oligonucleotide arrays to identify the mRNAs differentially expressed in the hippocampus of transgenic and wild-type mice. Keywords: Genetic modification, time course

2006-01-12 | GSE3965 | GEO