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Optogenetic control of the integrated stress response reveals proportional encoding and the stress memory landscape

ABSTRACT: Optogenetic control of the integrated stress response reveals proportional encoding and the stress memory landscape

PROVIDER: PRJNA863322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20701147_1.fastq.gz	Fastqsanger.gz
	SRR20701147_2.fastq.gz	Fastqsanger.gz
	SRR20701148_1.fastq.gz	Fastqsanger.gz
	SRR20701148_2.fastq.gz	Fastqsanger.gz
	SRR20701149_1.fastq.gz	Fastqsanger.gz

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Optogenetic control of the integrated stress response reveals proportional encoding and the stress memory landscape

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Project description:Understanding the mechanisms by which long-term memories are formed and stored in the brain represents a central aim of neuroscience. Prevailing theory suggests that long-term memory encoding involves early plasticity within hippocampal circuits, while reorganization of the neocortex is thought to occur weeks to months later to subserve remote memory storage. Here we report that long-term memory encoding can elicit early transcriptional, structural and functional remodeling of the neocortex. Parallel studies using genome-wide RNA-sequencing, ultrastructural imaging, and whole-cell recording in wild-type mice suggest that contextual fear conditioning initiates a transcriptional program in the medial prefrontal cortex (mPFC) that is accompanied by rapid expansion of the synaptic active zone and postsynaptic density, enhanced dendritic spine plasticity, and increased synaptic efficacy. To address the real-time contribution of the mPFC to long-term memory encoding, we performed temporally precise optogenetic inhibition of excitatory mPFC neurons during contextual fear conditioning. Using this approach, we found that real-time inhibition of the mPFC inhibited activation of the entorhinal-hippocampal circuit and impaired the formation of long-term associative memory. These findings suggest that encoding of long-term episodic memory is associated with early remodeling of neocortical circuits, identify the prefrontal cortex as a critical regulator of encoding-induced hippocampal activation and long-term memory formation, and have important implications for understanding memory processing in healthy and diseased brain states. 4 biological replicates per group were analyzed. The material analyzed was medial prefrontal cortex (mPFC; anterior cingulate cortex subregion) from both brain hemispheres, from which total RNA was extracted.

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Effects of optogenetic and chemogenetic LC activation on the hippocampal transcriptome

Project description:The locus coeruleus noradrenergic (LC-NA) system plays an important role in organizing a physiological response to acute stress. However, if and how the LC affects stress-mediated transcriptomic changes in the brain is still barely understood. Here, we extensively characterize LC mediated transcriptomic response during acute stress in the hippocampus. Combining for the first time bulk mRNA-sequencing and selective chemogenetic and optogenetic manipulations of the LC-NA system

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Optogenetic mitochondrial preconditioning enhances cardiomyocyte survival under stress

Project description:Mitochondria play a central role in preconditioning-mediated cytoprotection, yet the specific role of mitochondrial membrane potential (ΔΨm) in this process remains incompletely understood. In this study, we employed a next-generation, mitochondrial-targeted optogenetic system (mOpto) to induce precisely controlled (partial and transient) ΔΨm depolarization and investigate its role in enhancing cardiomyocyte resilience to stress. Human AC16 cardiomyocytes expressing mOpto were subjected to low-intensity LED illumination for preconditioning, followed by exposure to stressors including FCCP, H2O2, or simulated ischemia-reperfusion. mOpto-preconditioned cells exhibited significantly improved viability, attenuated ΔΨm depolarization, and reduced reactive oxygen species (ROS) production compared to non-preconditioned controls. Notably, this cytoprotective effect occurred independently of canonical ROS signaling and mitochondrial ATP-sensitive potassium channel (mitoKATP) activation. Transcriptional analysis revealed coordinated mitochondrial and metabolic reprogramming, including upregulation of genes involved in lipid biosynthesis, mitochondrial quality control, energy homeostasis, and a shift toward mitochondrial fusion. Importantly, mOpto preconditioning conferred similar cytoprotective effects in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), underscoring the translational potential of this approach. These findings demonstrate that mOpto-mediated transient ΔΨm depolarization induces a preconditioning effect that enhances cardiomyocyte resilience through the establishment of a mitochondrial "memory" and dynamic remodeling of mitochondrial function.

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Optogenetic neural stem cells microarray

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