Strategies and Tools for Studying Microglial-Mediated Synapse Elimination and Refinement

Morini, Raffaella; Bizzotto, Matteo; Perrucci, Fabio; Filipello, Fabia; Matteoli, Michela

doi:10.3389/fimmu.2021.640937

Cited by 16 publications

(9 citation statements)

References 194 publications

(176 reference statements)

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“…Microglia actively phagocytosed spines by forming SHF and physically pulling them away from the dendritic branch during microglia retraction. These observations are consistent with previous reports of microglia exhibiting phagocytosis, in which their processes elongate, retract, and physically pinch off fragments of membrane from other cells, or pull particles towards them (Kress et al, 2007;Morini et al, 2021;Takahashi et al, 2005;Weinhard et al, 2018).…”

Section: Discussionsupporting

confidence: 93%

Neuroinflammation triggers microglial phagocytosis of synapses via induction of synaptic filopodia

Cangalaya

Wegmann

Sun

et al. 2022

Preprint

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Activated microglia play a significant role in synaptic elimination during neuroinflammation, however, the events prior to the uptake of synaptic material by these cells remain elusive. Here, we performed in vivo two-photon imaging of microglia-synapse interactions in the context of systemic inflammation and Alzheimer´s disease. Both treatments induced microglial activation and decreased the basal surveillance of synapses by microglia. Focal synaptic stress was necessary to promote long-lasting microglia-neuron contacts and exacerbate spine elimination. The rate of spine elimination strongly correlated with the frequency of synaptic filopodia generation and microglial expression of phagocytic proteins. We show that activated microglia largely eliminate spines through phagocytosis rather than promoting their rapid retraction into dendrites. Moreover, we found that activated microglia induce the physical stretching of spines and their phagocytosis via the induction of spine head filopodia. Our real-time observations highlight key factors and decision points governing synaptic elimination by microglia during neuroinflammation.

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Section: Discussionsupporting

confidence: 93%

Neuroinflammation triggers microglial phagocytosis of synapses via induction of synaptic filopodia

Cangalaya

Wegmann

Sun

et al. 2022

Preprint

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“…Seeing the downregulation of microglial receptors related to phagocytic elimination of neuronal components, we next evaluated the phagocytic capacity of microglia by double-labeling of Iba1 and CD68 (Fig. 5e), a microglial lysosomal membrane protein [43]. In consensus with the downregulated phagocytic-related receptors, there was a signi cant decrease in the occupancy of CD68 within microglia in the NAcC but not the CPu in SD mice compared to NS controls (Fig.…”

Section: H Sd Decreased Microglial Phagocytic Capacity In the Striatummentioning

confidence: 96%

Sleep Deprivation Induces Dopamine System Maladaptation and Escalated Corticotrophin-Releasing Factor Signaling in Adolescent Mice

et al. 2023

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Sleep disruption is highly associated with the pathogenesis and progression of a wild range of psychiatric disorders. Furthermore, appreciable evidence shows that experimental sleep deprivation (SD) on humans and rodents evokes anomalies in the dopaminergic (DA) signaling, which are also implicated in the development of psychiatric illnesses such as schizophrenia or substance abuse. Since adolescence is a vital period for the maturation of the DA system as well as the occurrence of mental disorders, the present studies aimed to investigate the impacts of SD on the DA system of adolescent mice. We found that 72 h SD elicited a hyperdopaminergic status, with increased sensitivity to the novel environment and Amphetamine (Amph) challenge. Also, altered neuronal activity and expression of striatal DA receptors were noticed in the SD mice. Moreover, 72 h SD in uenced the immune status in the striatum, with reduced microglial phagocytic capacity, primed microglial activation, and neuroin ammation. The abnormal neuronal and microglial activity were putatively provoked by the enhanced corticotrophinreleasing factor (CRF) signaling and sensitivity during the SD period. Together, our ndings demonstrated the consequences of SD in adolescents including aberrant neuroendocrine, DA system, and in ammatory status. Sleep insu ciency is a risk factor for the aberration and neuropathology of psychiatric disorders.

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“…They subsequently produce proinflammatory molecules, including reactive oxygen species, reactive nitrogen species, inflammatory prostaglandins, and cytokines, including tumor necrosis factor alpha and interleukin-1beta [ 25 , 26 ]. In acquiring these properties, microglia may convert into phagocytic cells [ 27 ], and their activities facilitate the clearance of dead cells as well as other cell debris after damage, which are essential tasks in damage repair. Activated microglia use the complement system [ 28 ], also acquiring the capacity of delivering the antigen for T cells to perform their phagocytic function [ 29 ].…”

Section: Neuroinflammationmentioning

confidence: 99%

Infectious Microorganisms Seen as Etiologic Agents in Parkinson’s Disease

Stroe

Jurja

Mehedinți

et al. 2023

Life

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Infections represent a possible risk factor for parkinsonism and Parkinson’s disease (PD) based on information from epidemiology and fundamental science. The risk is unclear for the majority of agents. Moreover, the latency between infection and PD seems to be very varied and often lengthy. In this review, the evidence supporting the potential involvement of infectious microorganisms in the development of Parkinson’s disease is examined. Consequently, it is crucial to determine the cause and give additional treatment accordingly. Infection is an intriguing suggestion regarding the cause of Parkinson’s disease. These findings demonstrate that persistent infection with viral and bacterial microorganisms might be a cause of Parkinson’s disease. As an initiating factor, infection may generate a spectrum of gut microbiota dysbiosis, engagement of glial tissues, neuroinflammation, and alpha-synuclein accumulation, all of which may trigger and worsen the onset in Parkinson’s disease also contribute to its progression. Still uncertain is the primary etiology of PD with infection. The possible pathophysiology of PD infection remains a matter of debate. Furthermore, additional study is required to determine if PD patients develop the disease due to infectious microorganisms or solely since they are more sensitive to infectious causes.

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Strategies and Tools for Studying Microglial-Mediated Synapse Elimination and Refinement

Cited by 16 publications

References 194 publications

Neuroinflammation triggers microglial phagocytosis of synapses via induction of synaptic filopodia

Neuroinflammation triggers microglial phagocytosis of synapses via induction of synaptic filopodia

Sleep Deprivation Induces Dopamine System Maladaptation and Escalated Corticotrophin-Releasing Factor Signaling in Adolescent Mice

Infectious Microorganisms Seen as Etiologic Agents in Parkinson’s Disease

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