Astrocyte Heterogeneity in the Adult Central Nervous System

Miller, Sean

doi:10.3389/fncel.2018.00401

Cited by 165 publications

(142 citation statements)

References 37 publications

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“…Astroglia is known to be able to modulate the pain reaction intensity due to the production of cytokines, chemokines, and growth factors [Li et al, 2019]. At the same time, astrocytes, depending on the activation phenotype, can play a double role and exhibit neurotoxic or neuroprotective activity [Miller, 2018]. Phenotype A2 astrocytes exhibit neuroprotective properties, which inhibit neuroinflammation, promote tissue and membrane repair, accelerate cell proliferation, and inhibit apoptosis [Liddelow et al, 2017].…”

Section: Discussionmentioning

confidence: 99%

Neuropathic Pain Causes a Decrease in the Dendritic Tree Complexity of Hippocampal CA3 Pyramidal Neurons

Tyrtyshnaia

Manzhulo

Konovalova

et al. 2019

Cells Tissues Organs

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The International Pain Association defines neuropathic pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage." Recent studies show that chronic neuropathic pain causes both morphological and functional changes within brain structures. Due to the impact of supraspinal centers on pain signal processing, patients with chronic pain often suffer from depression, anxiety, memory impairment, and learning disabilities. Changes in hippocampal neuronal and glial plasticity can play a substantial role in the development of these symptoms. Given the special role of the CA3 hippocampal area in chronic stress reactions, we suggested that this region may undergo significant morphological changes as a result of persistent pain. Since the CA3 area is involved in the implementation of hippocampus-dependent memory, changes in the neuronal morphology can cause cognitive impairment observed in chronic neuropathic pain. This study aimed to elucidate the structural and plastic changes within the hippocampus associated with dendritic tree atrophy of CA3 pyramidal neurons in mice with chronic sciatic nerve constric-tion. Behavioral testing revealed impaired working and long-term memory in mice with a chronic constriction injury. Using the Golgi-Cox method, we revealed a decrease in the number of branches and dendritic length of CA3 pyramidal neurons. The dendritic spine number was decreased, predominantly due to a reduction in mushroom spines. An immunohistochemical study showed changes in astro-and microglial activity, which could affect the morphology of neurons both directly and indirectly via the regulation of neurotrophic factor synthesis. Using ELISA, we found a decrease in brain-derived neurotrophic factor production and an increase in neurotrophin-3 production. Morphological and biochemical changes in the CA3 area are accompanied by impaired working and long-term memory of animals. Thus, we can conclude that morphological and biochemical changes within the CA3 hippocampal area may underlie the cognitive impairment in neuropathic pain.

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Section: Discussionmentioning

confidence: 99%

Neuropathic Pain Causes a Decrease in the Dendritic Tree Complexity of Hippocampal CA3 Pyramidal Neurons

Tyrtyshnaia

Manzhulo

Konovalova

et al. 2019

Cells Tissues Organs

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“…Cre-negative samples most likely recapitulate the average translation in the analyzed region. With astrocytes being a highly abundant cell type in the CNS (Miller, 2018), it was not surprising that Cre-negative samples were most similar to GFAP samples ( Fig. 2c).…”

Section: Analysis Of Different Cns Cells Via Cell-type Specific Ribosmentioning

confidence: 93%

Prions induce minor genome-wide translational changes in neurons compared to glia

Scheckel

Imeri

Schwarz

et al. 2020

Preprint

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Prion diseases are caused by PrPSc, a self-replicating pathologically misfolded protein that exerts toxicity predominantly in the brain. The administration of PrPSc causes a robust, reproducible and specific disease manifestation. Here we have applied a combination of translating ribosome affinity purification and ribosome profiling to identify biologically relevant prion-induced changes during disease progression in a cell-type specific and genome-wide manner. Terminally diseased mice with severe neurological symptoms showed extensive alterations in astrocytes and microglia. Surprisingly, we detected only minor changes in the translational profiles of neurons. Prion-induced alterations in glia overlapped with those identified in other neurodegenerative diseases, suggesting that similar events occur in a broad spectrum of pathologies. Our results suggest that aberrant translation within glia may suffice to cause severe neurological symptoms and may even be the primary driver of prion disease.

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“…Astrocytes are the most abundant cell type in the brain, and participate to complex neuronal-glial interactions to assure synaptic homeostasis and metabolic sustainment for neurons (Miller, 2018). As for microglial cells, different phenotypes seem characterize astrocytic activation in physiological and pathological conditions, ranging from a pro-inflammatory A1 phenotype to a protective and anti-inflammatory A2 phenotype (Figure 1) (Miller, 2018).…”

Section: Pet and Mr Imaging Of Astrocytic Activationmentioning

confidence: 99%

Gliosis and Neurodegenerative Diseases: The Role of PET and MR Imaging

Cavaliere

Tramontano

Fiorenza

et al. 2020

Front. Cell. Neurosci.

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Glial activation characterizes most neurodegenerative and psychiatric diseases, often anticipating clinical manifestations and macroscopical brain alterations. Although imaging techniques have improved diagnostic accuracy in many neurological conditions, often supporting diagnosis, prognosis prediction and treatment outcome, very few molecular imaging probes, specifically focused on microglial and astrocytic activation, have been translated to a clinical setting. In this context, hybrid positron emission tomography (PET)/magnetic resonance (MR) scanners represent the most advanced tool for molecular imaging, combining the functional specificity of PET radiotracers (e.g., targeting metabolism, hypoxia, and inflammation) to both high-resolution and multiparametric information derived by MR in a single imaging acquisition session. This simultaneity of findings achievable by PET/MR, if useful for reciprocal technical adjustments regarding temporal and spatial cross-modal alignment/synchronization, opens still debated issues about its clinical value in neurological patients, possibly incompliant and highly variable from a clinical point of view. While several preclinical and clinical studies have investigated the sensitivity of PET tracers to track microglial (mainly TSPO ligands) and astrocytic (mainly MAOB ligands) activation, less studies have focused on MR specificity to this topic (e.g., through the assessment of diffusion properties and T2 relaxometry), and only few exploiting the integration of simultaneous hybrid acquisition. This review aims at summarizing and critically review the current state about PET and MR imaging for glial targets, as well as the potential added value of hybrid scanners for characterizing microglial and astrocytic activation.

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Astrocyte Heterogeneity in the Adult Central Nervous System

Cited by 165 publications

References 37 publications

Neuropathic Pain Causes a Decrease in the Dendritic Tree Complexity of Hippocampal CA3 Pyramidal Neurons

Neuropathic Pain Causes a Decrease in the Dendritic Tree Complexity of Hippocampal CA3 Pyramidal Neurons

Prions induce minor genome-wide translational changes in neurons compared to glia

Gliosis and Neurodegenerative Diseases: The Role of PET and MR Imaging

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