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

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

PROVIDER: PRJNA795353 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17480546.fastq.gz	Fastqsanger.gz
	SRR17480547.fastq.gz	Fastqsanger.gz
	SRR17480548.fastq.gz	Fastqsanger.gz
	SRR17480549.fastq.gz	Fastqsanger.gz
	SRR17480550.fastq.gz	Fastqsanger.gz

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

Project description:Impairment of long-term potentiation (LTP) is a common feature of many pre-clinical models of neurological disorders; however, studies in humans are limited by the inaccessibility of the brain. Human induced pluripotent stem cells (hiPSCs) provide a unique opportunity to study LTP in disease-specific genetic backgrounds. Here we describe a multi-electrode array (MEA)-based assay to investigate chemically induced LTP (cLTP) across entire networks of hiPSC-derived midbrain dopaminergic (DA) and cortical neuronal populations that lasts for days, allowing studies of the late phases of LTP and enabling detection of associated molecular changes. We show that cLTP on midbrain DA neuronal networks is largely independent of the N-methyl-D-aspartate receptor (NMDAR) and partially dependent on brain-derived neurotrophic factor (BDNF). Finally, we describe activity-regulated gene expression induced by cLTP. This cLTP-MEA assay platform will enable phenotype discovery and higher-throughput analyses of synaptic plasticity on hiPSC-derived neurons.

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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.

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