Glia Accumulate Evidence that Actions Are Futile and Suppress Unsuccessful Behavior DOI Creative Commons
Yu Mu, Davis Bennett, Mikail Rubinov

и другие.

Cell, Год журнала: 2019, Номер 178(1), С. 27 - 43.e19

Опубликована: Июнь 1, 2019

When a behavior repeatedly fails to achieve its goal, animals often give up and become passive, which can be strategic for preserving energy or regrouping between attempts. It is unknown how the brain identifies behavioral failures mediates this behavioral-state switch. In larval zebrafish swimming in virtual reality, visual feedback withheld so that swim attempts fail trigger expected flow. After tens of seconds such motor futility, became passive similar durations. Whole-brain calcium imaging revealed noradrenergic neurons responded specifically failed radial astrocytes whose levels accumulated with increasing numbers Using cell ablation optogenetic chemogenetic activation, we found progressively activated brainstem astrocytes, then suppressed swimming. Thus, perform computation critical behavior: they accumulate evidence current actions are ineffective consequently drive changes states. VIDEO ABSTRACT.

Язык: Английский

Calcium imaging reveals glial involvement in transcranial direct current stimulation-induced plasticity in mouse brain DOI Creative Commons
Hiromu Monai, Masamichi Ohkura,

Mika Tanaka

и другие.

Nature Communications, Год журнала: 2016, Номер 7(1)

Опубликована: Март 22, 2016

Abstract Transcranical direct current stimulation (tDCS) is a treatment known to ameliorate various neurological conditions and enhance memory cognition in humans. tDCS has gained traction for its potential therapeutic value; however, little about mechanism of action. Using transgenic mouse expressing G-CaMP7 astrocytes subpopulation excitatory neurons, we find that induces large-amplitude astrocytic Ca 2+ surges across the entire cortex with no obvious changes local field potential. Moreover, sensory evoked cortical responses are enhanced after tDCS. These enhancements dependent on alpha-1 adrenergic receptor not observed IP 3 R2 (inositol trisphosphate type 2) knockout mice, which absent. Together, propose metaplasticity through /IP signalling.

Язык: Английский

Процитировано

366

Human astrocytes: structure and functions in the healthy brain DOI Creative Commons
Flora Vasile, Elena Dossi, Nathalie Rouach

и другие.

Brain Structure and Function, Год журнала: 2017, Номер 222(5), С. 2017 - 2029

Опубликована: Март 9, 2017

Data collected on astrocytes' physiology in the rodent have placed them as key regulators of synaptic, neuronal, network, and cognitive functions. While these findings proved highly valuable for our awareness appreciation non-neuronal cell significance brain physiology, early structural phylogenic investigations human astrocytes hinted at potentially different astrocytic properties. This idea sparked interest to replicate rodent-based studies samples, which revealed an analogous but enhanced involvement neuronal function brain. Such evidence pointed a central role sustaining more complex information processing. Here, we review current state knowledge regarding their structure, gene profile, functions, highlighting differences with astrocytes. recent insight is essential assessment relevance using animal models comprehending functional species-specific properties Moreover, since dysfunctional been described many disorders, thorough understanding human-specific crucial better-adapted translational applications.

Язык: Английский

Процитировано

352

Astrocyte Heterogeneity: Impact to Brain Aging and Disease DOI Creative Commons
Isadora Matias,

Juliana Morgado,

Flávia Carvalho Alcântara Gomes

и другие.

Frontiers in Aging Neuroscience, Год журнала: 2019, Номер 11

Опубликована: Март 19, 2019

Astrocytes, one of the largest glial cell population in Central Nervous System, play key function several events brain development and function, such as synapse formation control neurotransmitters release uptake, production trophic factors neuronal survival. Initially described a homogenous population, evidences have pointed that astrocytes are highly heterogeneous, both morphologically functionally, within same region, across different regions. Recent findings suggest heterogeneity expression profile proteins involved astrocyte may predict selective vulnerability regions to specific diseases, well age-related cognitive decline. However, molecular mechanisms underlying these changes, either aging disease scarce. Neuroinflammation, hallmark neurodegenerative diseases aging, is reported dubious impact on activation, cells pro- anti-inflammatory cytokines chemokines, anti-oxidants, free radicals, neurotrophic factors. Despite emerging evidence supporting reactive duality their phenotype, neurotoxic or neuroprotective properties, depending age stimuli, cellular interplays regional still matter discussion. In this review, we will summarize recent phenotypes, likely for during neural diseases. We focus molecules triggered by Finally, discuss new how modulation phenotype could synaptic deficits dysfunction present pathological states.

Язык: Английский

Процитировано

329

Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells DOI Creative Commons
Denisa Kirdajová, Ján Kriška, Jana Turečková

и другие.

Frontiers in Cellular Neuroscience, Год журнала: 2020, Номер 14

Опубликована: Март 19, 2020

A plethora of neurological disorders shares a final common deadly pathway known as excitotoxicity. Among these disorders, ischemic injury is prominent cause death and disability worldwide. Brain ischemia stems from cardiac arrest or stroke, both responsible for insufficient blood supply to the brain parenchyma. Glucose oxygen deficiency disrupts oxidative phosphorylation, which results in energy depletion ionic imbalance, followed by cell membrane depolarization, calcium (Ca2+) overload, extracellular accumulation excitatory amino acid glutamate. If tight physiological regulation fails clear surplus this neurotransmitter, subsequent prolonged activation glutamate receptors forms vicious circle between elevated concentrations intracellular Ca2+ ions aberrant release, aggravating effect pathway. The downstream Ca2+-dependent enzymes has catastrophic impact on nervous tissue leading death, accompanied formation free radicals, edema, inflammation. After decades "neuron-centric" approaches, recent research also finally shed some light role glial cells diseases. It becoming more evident that neurons glia depend each other. Neuronal cells, astrocytes, microglia, NG2 glia, oligodendrocytes all have their roles what However, who main contributor pathway, unsuspecting victim? In review article, we summarize so-far-revealed central system, with particular attention ischemia-induced excitotoxicity, its origins, consequences.

Язык: Английский

Процитировано

319

Glia Accumulate Evidence that Actions Are Futile and Suppress Unsuccessful Behavior DOI Creative Commons
Yu Mu, Davis Bennett, Mikail Rubinov

и другие.

Cell, Год журнала: 2019, Номер 178(1), С. 27 - 43.e19

Опубликована: Июнь 1, 2019

When a behavior repeatedly fails to achieve its goal, animals often give up and become passive, which can be strategic for preserving energy or regrouping between attempts. It is unknown how the brain identifies behavioral failures mediates this behavioral-state switch. In larval zebrafish swimming in virtual reality, visual feedback withheld so that swim attempts fail trigger expected flow. After tens of seconds such motor futility, became passive similar durations. Whole-brain calcium imaging revealed noradrenergic neurons responded specifically failed radial astrocytes whose levels accumulated with increasing numbers Using cell ablation optogenetic chemogenetic activation, we found progressively activated brainstem astrocytes, then suppressed swimming. Thus, perform computation critical behavior: they accumulate evidence current actions are ineffective consequently drive changes states. VIDEO ABSTRACT.

Язык: Английский

Процитировано

313