Lighting Up Ca2+ Dynamics in Animal Models

Redolfi, Nelly; García-Casas, Paloma; Fornetto, Chiara; Sonda, Sonia; Pizzo, Paola; Pendin, Diana

doi:10.3390/cells10082133

Cited by 6 publications

(3 citation statements)

References 226 publications

(270 reference statements)

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“…This new toolkit comprises sensors selective for modulatory ligands, reporters of GPCR and G protein activation, abilities to eavesdrop on numerous second-messenger systems and measure ion channel function. Here we can cite just a small sampling of an impressive decade's landmarks and reviews (Banghart and Sabatini, 2012;Irannejad et al, 2013Irannejad et al, , 2014Tsvetanova and von Zastrow, 2014;Spangler and Bruchas, 2017;Banghart et al, 2018;Patriarchi et al, 2019;Zeng et al, 2019;Ravotto et al, 2020;Sabatini and Tian, 2020;Smith et al, 2020;Stoeber et al, 2020;Unger et al, 2020;Jullie et al, 2021;Labouesse and Patriarchi, 2021;Redolfi et al, 2021;Tjahjono et al, 2021), while offering also a small sampling of progress emerging just at the time of this writing (Condon et al, 2021;Copits et al, 2021;Melzer et al, 2021;Wan et al, 2021;Duffet et al, 2022;Qian et al, 2022;Wu et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

A Molecular Landscape of Mouse Hippocampal Neuromodulation

Smith

Zastrow

2022

Front. Neural Circuits

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Adaptive neuronal circuit function requires a continual adjustment of synaptic network parameters known as “neuromodulation.” This process is now understood to be based primarily on the binding of myriad secreted “modulatory” ligands such as dopamine, serotonin and the neuropeptides to G protein-coupled receptors (GPCRs) that, in turn, regulate the function of the ion channels that establish synaptic weights and membrane excitability. Many of the basic molecular mechanisms of neuromodulation are now known, but the organization of neuromodulation at a network level is still an enigma. New single-cell RNA sequencing data and transcriptomic neurotaxonomies now offer bright new lights to shine on this critical “dark matter” of neuroscience. Here we leverage these advances to explore the cell-type-specific expression of genes encoding GPCRs, modulatory ligands, ion channels and intervening signal transduction molecules in mouse hippocampus area CA1, with the goal of revealing broad outlines of this well-studied brain structure’s neuromodulatory network architecture.

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Section: Discussionmentioning

confidence: 99%

A Molecular Landscape of Mouse Hippocampal Neuromodulation

Smith

Zastrow

2022

Front. Neural Circuits

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“…Ca 2+ imaging is a powerful and widely used approach (Patriarchi et al, 2018;Corkrum et al, 2020;Redolfi et al, 2021) and, thus far, preferred over fluorescent voltage indicators due to superior sensitivity, kinetics, and ease of expression (Vogt, 2015;Inagaki and Nagai, 2016;Mollinedo-Gajate et al, 2019;Inoue, 2021;Zhu et al, 2021). Ca 2+ imaging utilizes fluorescent calcium indicators, often encoded by transgenes with neuron specific promoters, enabling selective labeling in nervous system areas with high cellular heterogeneity.…”

Section: Introductionmentioning

confidence: 99%

Reduced Ca2+ transient amplitudes may signify increased or decreased depolarization depending on the neuromodulatory signaling pathway

2022

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Neuromodulators regulate neuronal excitability and bias neural circuit outputs. Optical recording of neuronal Ca2+ transients is a powerful approach to study the impact of neuromodulators on neural circuit dynamics. We are investigating the polymodal nociceptor ASH in Caenorhabditis elegans to better understand the relationship between neuronal excitability and optically recorded Ca2+ transients. ASHs depolarize in response to the aversive olfactory stimulus 1-octanol (1-oct) with a concomitant rise in somal Ca2+, stimulating an aversive locomotory response. Serotonin (5-HT) potentiates 1-oct avoidance through Gαq signaling, which inhibits L-type voltage-gated Ca2+ channels in ASH. Although Ca2+ signals in the ASH soma decrease, depolarization amplitudes increase because Ca2+ mediates inhibitory feedback control of membrane potential in this context. Here, we investigate octopamine (OA) signaling in ASH to assess whether this negative correlation between somal Ca2+ and depolarization amplitudes is a general phenomenon, or characteristic of certain neuromodulatory pathways. Like 5-HT, OA reduces somal Ca2+ transient amplitudes in ASH neurons. However, OA antagonizes 5-HT modulation of 1-oct avoidance behavior, suggesting that OA may signal through a different pathway. We further show that the pathway for OA diminution of ASH somal Ca2+ consists of the OCTR-1 receptor, the Go heterotrimeric G-protein, and the G-protein activated inwardly rectifying channels IRK-2 and IRK-3, and this pathway reduces depolarization amplitudes in parallel with somal Ca2+ transient amplitudes. Therefore, even within a single neuron, somal Ca2+ signal reduction may indicate either increased or decreased depolarization amplitude, depending on which neuromodulatory signaling pathways are activated, underscoring the need for careful interpretation of Ca2+ imaging data in neuromodulatory studies.

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“…Adequate fluorescence at basal cell [Ca 2+ ] (XCaMP-G). Enables measurement of fast-spike trains in individual neurons Inoue et al, 2019;Redolfi et al, 2021.…”

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confidence: 99%

Advancements in the Quest to Map, Monitor, and Manipulate Neural Circuitry

Swanson

Chin

Romero

et al. 2022

Front. Neural Circuits

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Neural circuits and the cells that comprise them represent the functional units of the brain. Circuits relay and process sensory information, maintain homeostasis, drive behaviors, and facilitate cognitive functions such as learning and memory. Creating a functionally-precise map of the mammalian brain requires anatomically tracing neural circuits, monitoring their activity patterns, and manipulating their activity to infer function. Advancements in cell-type-specific genetic tools allow interrogation of neural circuits with increased precision. This review provides a broad overview of recombination-based and activity-driven genetic targeting approaches, contemporary viral tracing strategies, electrophysiological recording methods, newly developed calcium, and voltage indicators, and neurotransmitter/neuropeptide biosensors currently being used to investigate circuit architecture and function. Finally, it discusses methods for acute or chronic manipulation of neural activity, including genetically-targeted cellular ablation, optogenetics, chemogenetics, and over-expression of ion channels. With this ever-evolving genetic toolbox, scientists are continuing to probe neural circuits with increasing resolution, elucidating the structure and function of the incredibly complex mammalian brain.

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Lighting Up Ca2+ Dynamics in Animal Models

Cited by 6 publications

References 226 publications

A Molecular Landscape of Mouse Hippocampal Neuromodulation

A Molecular Landscape of Mouse Hippocampal Neuromodulation

Reduced Ca2+ transient amplitudes may signify increased or decreased depolarization depending on the neuromodulatory signaling pathway

Advancements in the Quest to Map, Monitor, and Manipulate Neural Circuitry

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