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Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and synaptic plasticity

ABSTRACT: Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and synaptic plasticity

PROVIDER: PRJNA419889 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6324120_1.fastq.gz	Fastqsanger.gz
	SRR6324120_2.fastq.gz	Fastqsanger.gz
	SRR6324111_1.fastq.gz	Fastqsanger.gz
	SRR6324111_2.fastq.gz	Fastqsanger.gz
	SRR6324121_1.fastq.gz	Fastqsanger.gz

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Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and synaptic plasticity

Project description:Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and synaptic plasticity

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Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and synaptic plasticity

Project description:Clinical trials are currently underway to assess the efficacy of forniceal deep brain stimulation (DBS) for the improvement of memory in Alzheimer’s patients, and forniceal DBS has been shown to improve learning and memory in a mouse model of Rett syndrome (RTT), an intellectual disability disorder. The mechanism of DBS benefits has been elusive, however, so we assessed gene expression, splice isoform abundance, DNA methylation, and proteomic changes following acute forniceal DBS in wild-type mice and a mouse model lacking Mecp2, the gene whose loss of function causes RTT. We found that DBS upregulates genes involved in synaptic function, cell survival, and neurogenesis, and alters the proportions of different isoforms even for genes whose expression is unchanged. DBS rescued ~25% of the gene expression defects in Mecp2-null mice, particularly those involved in synaptic components, and it induced expression of 17-24% of the genes found to be downregulated in intellectual disability mouse models and in post-mortem human brain tissue from patients with Major Depressive Disorder. DBS could thus benefit individuals with a variety of neuropsychiatric disorders.

2018-04-17 | GSE107383 | GEO

Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and synaptic plasticity

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Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and plasticity

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Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and plasticity

Project description:Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and plasticity

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Distinct contributions of ventral CA1/amygdala co-activation to the induction and maintenance of synaptic plasticity

Project description:The amygdala is known to modulate hippocampal synaptic plasticity. One role could be an immediate effect of basolateral amygdala (BLA) in priming synaptic plasticity in the hippocampus. Another role could be through associative synaptic co-operation and competition that triggers events involved in the maintenance of synaptic potentiation. We present evidence that the timing and activity level of BLA stimulation are important factors for the induction and maintenance of long-term potentiation (LTP) in ventral hippocampal area CA1. A 100 Hz BLA co-stimulation facilitated the induction of LTP, whereas 200 Hz co-stimulation attenuated induction. A 100 Hz BLA co-stimulation also caused enhanced persistence, sufficient to prevent synaptic competition. This maintenance effect is likely through translational mechanisms, as mRNA expression of primary response genes was unaffected, whereas protein level of plasticity-related products was increased. Further understanding of the neural mechanisms of amygdala modulation on hippocampus could provide insights into the mechanisms of emotional disorders.

2022-03-03 | GSE197708 | GEO

NRBF2 orchestrates autophagic flux and adult hippocampal neurogenesis in chronic stress-induced depression

Project description:By precisely dissected LC-MS/MS for proteomics and phosphoproteomics, we found that deletion of NRBF2 disrupts neurogenesis-related protein network in the DG, such as neurogenesis, cell development, cell morphogenesis, cellular homeostasis, and synaptic plasticity.

2023-10-24 | PXD034382 | Pride

Forniceal deep brain stimulation induces gene expression and splicing changes that promote neurogenesis and plasticity.

Project description:Clinical trials are currently underway to assess the efficacy of forniceal deep brain stimulation (DBS) for improvement of memory in Alzheimer's patients, and forniceal DBS has been shown to improve learning and memory in a mouse model of Rett syndrome (RTT), an intellectual disability disorder caused by loss-of-function mutations in MECP2. The mechanism of DBS benefits has been elusive, however, so we assessed changes in gene expression, splice isoforms, DNA methylation, and proteome following acute forniceal DBS in wild-type mice and mice lacking Mecp2. We found that DBS upregulates genes involved in synaptic function, cell survival, and neurogenesis and normalized expression of ~25% of the genes altered in Mecp2-null mice. Moreover, DBS induced expression of 17-24% of the genes downregulated in other intellectual disability mouse models and in post-mortem human brain tissue from patients with Major Depressive Disorder, suggesting forniceal DBS could benefit individuals with a variety of neuropsychiatric disorders.

| S-EPMC5906096 | biostudies-literature

Chronic administration of non-constitutive proteasome inhibitor modulates plasticity in hippocampus following tetanic stimulation, but not short theta-burst stimulation.

Project description:Proteasomes degrade most intracellular proteins. Several different forms of proteasomes are known. Proteasome inhibitors targeting different proteasome forms are used in clinical practice and were shown to modulate long-term potentiation (LTP) in hippocampal slices of untreated animals. Here we studied the effect of chronic administration of non-constitutive proteasome inhibitor ONX-0914 on the LTP induced by two different protocols: tetanic stimulation and theta-burst stimulation (TBS). Excitatory postsynaptic potentials (fEPSPs) in hippocampal slices from control animals and animals treated with DMSO or ONX-0914 were compared. The TBS stimulation did not change LTP kinetics in hippocampal slices, however chronic administration of ONX-0914 led to the decrease in fEPSP slopes after tetanic stimulation. Observed effects correlated with differential expression of genes involved in synaptic plasticity, glutaminergic synapse and synaptic signaling. Obtained results indicate that non-constitutive proteasomes are likely involved in the tetanus-evoked LTP but not the LTP occurring after TBS, supporting the relevance and complexity of the role of proteasomes in the synaptic plasticity.

2023-04-05 | GSE229000 | GEO

Astrocyte-secreted IL-33 mediates homeostatic synaptic plasticity in the adult hippocampus

Project description:Hippocampal synaptic plasticity is important for learning and memory formation. Homeostatic synaptic plasticity is a specific form of synaptic plasticity that is induced upon prolonged changes in neuronal activity to maintain network homeostasis. While astrocytes are important regulators of synaptic transmission and plasticity, it is largely unclear how they interact with neurons to regulate synaptic plasticity at the circuit level. Here, we show that neuronal activity blockade selectively increases the expression and secretion of IL-33 (interleukin-33) by astrocytes in the hippocampal cornu ammonis 1 (CA1) subregion. This IL-33 stimulates an increase in excitatory synapses and neurotransmission through the activation of neuronal IL-33 receptor complex and synaptic recruitment of the scaffold protein PSD-95. We found that acute administration of tetrodotoxin in hippocampal slices or inhibition of hippocampal CA1 excitatory neurons by optogenetic manipulation increases IL-33 expression in CA1 astrocytes. Furthermore, IL-33 administration in vivo promotes the formation of functional excitatory synapses in hippocampal CA1 neurons, whereas conditional knockout of IL-33 in CA1 astrocytes decreases the number of excitatory synapses therein. Importantly, blockade of IL-33 and its receptor signaling in vivo by intracerebroventricular administration of its decoy receptor inhibits homeostatic synaptic plasticity in CA1 pyramidal neurons and impairs spatial memory formation in mice. These results collectively reveal an important role of astrocytic IL-33 in mediating the negative-feedback signaling mechanism in homeostatic synaptic plasticity, providing insights into how astrocytes maintain hippocampal network homeostasis.

2020-12-14 | GSE161540 | GEO

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