The Participation of Microglia in Neurogenesis: A Review

Pérez-Rodríguez, Diego R.; Blanco‐Luquin, Idoia; Mendioroz, Maite

doi:10.3390/brainsci11050658

Cited by 38 publications

(26 citation statements)

References 102 publications

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“…Recent studies have indicated the role of neuron-microglia interaction in the function and maturation of glutamatergic synapse and demonstrated how microglia influence synaptic organizations and activity [111,112]. Moreover, Perez-Rodriguez described the role of microglia in neurogenesis in the adult brain [113]. Despite all studies, the physiological function of microglial cells and their interplay with neurons in the brain is not fully elucidated.…”

Section: Glutamatergic Signaling In Microglia-neuron Communication In Admentioning

confidence: 99%

Glutamate and GABA in Microglia-Neuron Cross-Talk in Alzheimer’s Disease

Czapski

Strosznajder

2021

IJMS

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The physiological balance between excitation and inhibition in the brain is significantly affected in Alzheimer’s disease (AD). Several neuroactive compounds and their signaling pathways through various types of receptors are crucial in brain homeostasis, among them glutamate and γ-aminobutyric acid (GABA). Activation of microglial receptors regulates the immunological response of these cells, which in AD could be neuroprotective or neurotoxic. The novel research approaches revealed the complexity of microglial function, including the interplay with other cells during neuroinflammation and in the AD brain. The purpose of this review is to describe the role of several proteins and multiple receptors on microglia and neurons, and their involvement in a communication network between cells that could lead to different metabolic loops and cell death/survival. Our review is focused on the role of glutamatergic, GABAergic signaling in microglia–neuronal cross-talk in AD and neuroinflammation. Moreover, the significance of AD-related neurotoxic proteins in glutamate/GABA-mediated dialogue between microglia and neurons was analyzed in search of novel targets in neuroprotection, and advanced pharmacological approaches.

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Section: Glutamatergic Signaling In Microglia-neuron Communication In Admentioning

confidence: 99%

Glutamate and GABA in Microglia-Neuron Cross-Talk in Alzheimer’s Disease

Czapski

Strosznajder

2021

IJMS

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“…Microglia, known as “brain gardeners,” have been found to influence neuronal proliferation, differentiation, and maturation [ 65 , 66 , 67 ]. Microglial morphology is closely linked to microglial functions [ 68 , 69 ], and changes in microglial phenotype are related to the impairment of hippocampal neurogenesis under pathological conditions [ 70 ].…”

Section: Discussionmentioning

confidence: 99%

High-Fat Diet Consumption in Adolescence Induces Emotional Behavior Alterations and Hippocampal Neurogenesis Deficits Accompanied by Excessive Microglial Activation

Yao

Yang

Wang

et al. 2022

IJMS

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Adolescence is a developmental epoch characterized by massive neural circuit remodeling; thus, the brain is particularly vulnerable to environmental influences during this period. Excessive high-fat diet (HFD) consumption, which is very common among adolescents, has long been recognized as a potent risk factor for multiple mood disorders, including depression and anxiety. However, the precise mechanisms underlying the influences of HFD consumption in adolescence on emotional health are far from clear. In the present study, C57BL/6 mice were fed a control diet (CD) or HFD for about 4 weeks from postnatal day (P) 28 to P60, spanning most of the adolescence period, and then subjected to behavioral assessments and histological examinations. HFD mice exhibited elevated levels of depression and anxiety, decreased hippocampal neurogenesis, and excessive microglial activation in the ventral hippocampus. Furthermore, in HFD-fed mice, microglia showed increased DCX+ inclusions, suggesting aberrant microglial engulfment of newborn neurons in HFD-fed adolescents. To our knowledge, this is the first observation suggesting that the negative effects of HFD consumption in adolescence on emotion and neuroplasticity may be attributed at least in part to aberrant microglial engulfment of nascent neurons, extending our understanding of the mechanism underlying HFD-related affective disorders in young people.

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“…Microglia are macrophage-like cells in the CNS that have the function of maintaining homeostasis under physiological conditions. , Sensitization of microglia is a vital part of the pathogenesis of inflammatory pain. − Tissue injury activates microglia, which secretes a variety of pro-inflammatory cytokines, such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α). , The discharge of these pro-inflammatory cytokines promotes the persistence of behavioral hypersensitivity reactions after injury or surrounding inflammation and plays an influential role in chronic inflammatory pain . In the spinal cord ischemia–reperfusion model, the increased expression of the chemokine C-X-C motif ligand 10 (CXCL10) led to overexpression of the chemokine receptor C-X-C motif receptor 3 (CXCR3) and stimulated the sensitization of microglia and the release of pro-inflammatory cytokines, eventually enlarging the inflammatory cascade and pain process .…”

Section: Glial Cells In the Central Nervous System And Inflammatory Painmentioning

confidence: 99%

A Novel Progress: Glial Cells and Inflammatory Pain

Wang

2022

ACS Chem. Neurosci.

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Inflammatory pain is the perception of noxious stimuli that occurs during inflammation or an immune response. Glial cells are widespread in the central and peripheral nervous systems, supporting and guiding the migration of neurons, participating in the immune response, forming the myelin sheath and blood–brain barrier, and maintaining the concentration of potassium ions outside nerve cells. Recent studies have shown that glial cells have a significant connection with the production and development of inflammatory pain. This article reviews the relationship, mechanisms, therapeutic targets between five types of glial cells and inflammatory pain, and the medicine composition that can effectively inhibit inflammatory pain. It expands the study on the mechanism of glial cells regulating pain and provides new ideas for the therapy of inflammatory pain.

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The Participation of Microglia in Neurogenesis: A Review

Cited by 38 publications

References 102 publications

Glutamate and GABA in Microglia-Neuron Cross-Talk in Alzheimer’s Disease

Glutamate and GABA in Microglia-Neuron Cross-Talk in Alzheimer’s Disease

High-Fat Diet Consumption in Adolescence Induces Emotional Behavior Alterations and Hippocampal Neurogenesis Deficits Accompanied by Excessive Microglial Activation

A Novel Progress: Glial Cells and Inflammatory Pain

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