Modern Microglia: Novel Targets in Psychiatric Neuroscience

Dwyer, Jennifer B.; Ross, David A.

doi:10.1016/j.biopsych.2016.08.006

Cited by 15 publications

(24 citation statements)

References 11 publications

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“…Briefly, microglia respond to insult in two main ways: they increase in number in the affected area and their morphology (cell body size and extension number/size) alter (Kettenmann et al, 2011; Calcia et al, 2016). Resting (ramified) microglia in a healthy CNS system have a small cell body and long, thin extensions, with many processes (Kettenmann et al, 2011; Calcia et al, 2016; Dwyer and Ross, 2016). In this ramified stage microglia search for signals of insult (Kettenmann et al, 2011; Walker et al, 2014; Dwyer and Ross, 2016).…”

Section: Introductionmentioning

confidence: 99%

“…Resting (ramified) microglia in a healthy CNS system have a small cell body and long, thin extensions, with many processes (Kettenmann et al, 2011; Calcia et al, 2016; Dwyer and Ross, 2016). In this ramified stage microglia search for signals of insult (Kettenmann et al, 2011; Walker et al, 2014; Dwyer and Ross, 2016). Upon detection of harmful stimuli, microglia number increase in the affected area, and morphology alter to become amoeboid, with most notable changes being an increase in cell body size, and reduced branching, and number of extensions (Kettenmann et al, 2011; Walker et al, 2014; Dwyer and Ross, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Contextual Fear Conditioning Alter Microglia Number and Morphology in the Rat Dorsal Hippocampus

Chaaya

Jacques

Belmer

et al. 2019

Front. Cell. Neurosci.

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Contextual fear conditioning is a Pavlovian conditioning paradigm capable of rapidly creating fear memories to contexts, such as rooms or chambers. Contextual fear conditioning protocols have long been utilized to evaluate how fear memories are consolidated, maintained, expressed, recalled, and extinguished within the brain. These studies have identified the lateral portion of the amygdala and the dorsal portion of the hippocampus as essential for contextual fear memory consolidation. The current study was designed to evaluate how two different contextual fear memories alter amygdala and hippocampus microglia, brain derived neurotrophic factor (BDNF), and phosphorylated cyclic-AMP response element binding (pCREB). We find rats provided with standard contextual fear conditioning to have more microglia and more cells expressing BDNF in the dentate gyrus as compared to a context only control group. Additionally, standard contextual fear conditioning altered microglia morphology to become amoeboid in shape – a common response to central nervous system insult, such as traumatic brain injury, infection, ischemia, and more. The unpaired fear conditioning procedure (whereby non-reinforced and non-overlapping auditory tones were provided at random intervals during conditioning), despite producing equivalent levels of fear as the standard procedure, did not alter microglia, BDNF or pCREB number in any dorsal hippocampus or lateral amygdala brain regions. Despite this, the unpaired fear conditioning protocol produced some alterations in microglia morphology, but less compared to rats provided with standard contextual fear conditioning. Results from this study demonstrate that contextual fear conditioning is capable of producing large alterations to dentate gyrus plasticity and microglia, whereas unpaired fear conditioning only produces minor changes to microglia morphology. These data show, for the first time, that Pavlovian fear conditioning protocols can induce similar responses as trauma, infection or other insults within the central nervous system.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Contextual Fear Conditioning Alter Microglia Number and Morphology in the Rat Dorsal Hippocampus

Chaaya

Jacques

Belmer

et al. 2019

Front. Cell. Neurosci.

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“…Under normal circumstances, microglia are in a resting state, receive synaptic signals by sensing changes in the extracellular environment, thereby participating in intersynaptic interactions; and can also express neurotransmitters such as dopamine and serotonin. When the extracellular environment changes, microglia can be activated and undergo morphological changes, releasing inflammatory factors (38). Activated microglia are divided into two polarization states, M1 and M2.…”

Section: Etiologies Of Psdmentioning

confidence: 99%

Diversiform Etiologies for Post-stroke Depression

et al. 2019

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After the onset of stroke, many patients suffer from emotional behavior changes. Approximately, one-third of stroke survivors are affected by post-stroke depression (PSD), making it a serious social and public health problem. Post-stroke depression (PSD) has an important impact on the course, recovery, and prognosis of stroke. The pathogenesis of PSD is very complex, involving many factors such as biological mechanism and social psychological mechanisms. This article provides a brief review of the hot issues related to etiologies of PSD.

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“…Microglia are the main immune cells in the CNS and can function as macrophages in the brain (Ginhoux et al, 2013). In serious neuropathological conditions, microglia can be activated and secrete proinflammatory cytokines and neurotoxic mediators, such as TNF-α, IL-6, IL-1β, NO and ROS, which cause additional neuroinflammation and aggravate brain disease progression (Biber et al, 2014; Brown and Vilalta, 2015; Dwyer and Ross, 2016; Beckers et al, 2018). Activated microglia have been found in the cerebral cortex, hippocampus and pituitary gland of the brain in heat stroke animal models.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-155 Promotes Heat Stress-Induced Inflammation via Targeting Liver X Receptor α in Microglia

Gong

Zhang

et al. 2019

Front. Cell. Neurosci.

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Background: The neuroinflammatory responses of microglial cells play an important role in the process of brain dysfunction caused by heat stroke. MicroRNAs are reportedly involved in a complex signaling network and have been identified as neuroinflammatory regulators. In this study, we determined the biological roles of microRNA-155 in the inflammatory responses in heat-stressed microglia and explored the underlying mechanisms.Methods: MicroRNA-155 mimic and inhibitor were used to separately upregulate or downregulate microRNA-155 expression. The activation state of BV-2 microglial cells (BV-2 cells) was assessed via immunoreactions using the microglial marker CD11b and CD68. Levels of induced interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured using real-time reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assays (ELISAs). The activation of nuclear factor kappa B (NF-κB) signaling proteins was evaluated by Western blotting for inhibitory kappa B alpha (IκBα) and NF-κB p65 phosphorylation and indirect immunofluorescence analysis using a p65 phosphorylation antibody. A luciferase reporter assay was used to verify liver X receptor α (LXRα) as a target gene of microRNA-155.Results: Heat stress significantly induced IL-1β, IL-6, and TNF-α release and increased the expression of CD11b and CD68. In addition, IκBα and NF-κB p65 phosphorylation were dramatically increased by heat stress, and microRNA-155 expression was also elevated. High expression of microRNA-155 in heat-stressed microglial cells was inversely correlated with LXRα expression. We then determined the role of microRNA-155 in the heat stress-induced inflammatory responses. The results revealed that by targeting LXRα, microRNA-155 enhanced NF-κB signaling activation and facilitated immune inflammation in heat stress-treated BV-2 cells.Conclusion: MicroRNA-155 promotes heat stress-induced inflammatory responses in microglia. The underlying mechanisms may include facilitating inflammatory factors expression by increasing NF-κB pathway activation via targeting LXRα.

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Modern Microglia: Novel Targets in Psychiatric Neuroscience

Cited by 15 publications

References 11 publications

Contextual Fear Conditioning Alter Microglia Number and Morphology in the Rat Dorsal Hippocampus

Contextual Fear Conditioning Alter Microglia Number and Morphology in the Rat Dorsal Hippocampus

Diversiform Etiologies for Post-stroke Depression

MicroRNA-155 Promotes Heat Stress-Induced Inflammation via Targeting Liver X Receptor α in Microglia

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