scholarly journals Comparative Review of Microglia and Monocytes in CNS Phagocytosis

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2555
Author(s):  
Megumi Andoh ◽  
Ryuta Koyama
Keyword(s):  
Neural Circuit ◽  
Future Research ◽  
Phagocytic Cells ◽  
Research Directions ◽  
Microglial Phagocytosis ◽  
Neuronal Synapses ◽  
Comparative Review ◽  
The Central Nervous System ◽  
Future Research Directions ◽  
Circuit Function

Macrophages maintain tissue homeostasis by phagocytosing and removing unwanted materials such as dead cells and cell debris. Microglia, the resident macrophages of the central nervous system (CNS), are no exception. In addition, a series of recent studies have shown that microglia phagocytose the neuronal synapses that form the basis of neural circuit function. This discovery has spurred many neuroscientists to study microglia. Importantly, in the CNS parenchyma, not only microglia but also blood-derived monocytes, which essentially differentiate into macrophages after infiltration, exert phagocytic ability, making the study of phagocytosis in the CNS even more interesting and complex. In particular, in the diseased brain, the phagocytosis of tissue-damaging substances, such as myelin debris in multiple sclerosis (MS), has been shown to be carried out by both microglia and blood-derived monocytes. However, it remains largely unclear why blood-derived monocytes need to invade the parenchyma, where microglia are already abundant, to assist in phagocytosis. We will also discuss whether this phagocytosis can affect the fate of the phagocytosing cell itself as well as the substance being phagocytosed and the surrounding environment in addition to future research directions. In this review, we will introduce recent studies to answer a question that often arises when studying microglial phagocytosis: under what circumstances and to what extent blood-derived monocytes infiltrate the CNS and contribute to phagocytosis. In addition, the readers will learn how recent studies have experimentally distinguished between microglia and infiltrating monocytes. Finally, we aim to contribute to the progress of phagocytosis research by discussing the effects of phagocytosis on phagocytic cells.

scholarly journals Cannabinoid Signaling in the Skin: Therapeutic Potential of the “C(ut)annabinoid” System

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 918 ◽  
Author(s):  
Kinga Tóth ◽  
Dorottya Ádám ◽  
Tamás Bíró ◽  
Attila Oláh
Keyword(s):  
Therapeutic Potential ◽  
Endocannabinoid System ◽  
The Body ◽  
Future Research ◽  
Research Directions ◽  
Physiological Processes ◽  
Barrier Formation ◽  
The Central Nervous System ◽  
Future Research Directions ◽  
Pigmentation Disorders

The endocannabinoid system (ECS) has lately been proven to be an important, multifaceted homeostatic regulator, which influences a wide-variety of physiological processes all over the body. Its members, the endocannabinoids (eCBs; e.g., anandamide), the eCB-responsive receptors (e.g., CB1, CB2), as well as the complex enzyme and transporter apparatus involved in the metabolism of the ligands were shown to be expressed in several tissues, including the skin. Although the best studied functions over the ECS are related to the central nervous system and to immune processes, experimental efforts over the last two decades have unambiguously confirmed that cutaneous cannabinoid (“c[ut]annabinoid”) signaling is deeply involved in the maintenance of skin homeostasis, barrier formation and regeneration, and its dysregulation was implicated to contribute to several highly prevalent diseases and disorders, e.g., atopic dermatitis, psoriasis, scleroderma, acne, hair growth and pigmentation disorders, keratin diseases, various tumors, and itch. The current review aims to give an overview of the available skin-relevant endo- and phytocannabinoid literature with a special emphasis on the putative translational potential, and to highlight promising future research directions as well as existing challenges.

scholarly journals Synapse development is regulated by microglial THIK-1 K+ channels

2021 ◽  
Author(s):  
Pablo Izquierdo ◽  
Hiroko Shiina ◽  
Chanawee Hirunpattarasilp ◽  
Huma Sethi ◽  
David Attwell
Keyword(s):  
Neural Circuit ◽  
Brain Slices ◽  
Brain Parenchyma ◽  
Glutamatergic Synapses ◽  
Synaptic Density ◽  
Microglial Phagocytosis ◽  
Disease States ◽  
The Central Nervous System ◽  
Circuit Function ◽  
Dying Cells

Microglia are the resident immune cells of the central nervous system. They constantly survey the brain parenchyma for redundant synapses, debris or dying cells, which they remove through phagocytosis. Microglial ramification, motility and cytokine release are regulated by tonically active THIK-1 K+ channels on the microglial plasma membrane. Here, we examined whether these channels play a role in phagocytosis. Using pharmacological blockers and THIK-1 knockout (KO) mice, we found that lack of THIK-1 activity reduced microglial phagocytosis, which may result in impaired pruning of synapses. In hippocampus, mice lacking THIK-1 expression had an increased number of glutamatergic synapses during development. This resulted from an increased number of presynaptic terminals, due to impaired removal by THIK-1 KO microglia. In microglia in brain slices from fresh human biopsies, modulating THIK-1 function had effects similar to those in rodents: blocking THIK-1 rapidly reduced microglial process ramification and increased synaptic density. The dependence of synapse number on THIK-1 K+ channels, which control microglial surveillance and phagocytic ability, implies that changes in THIK-1 expression level over the lifespan or in disease states may contribute to altering neural circuit function.

scholarly journals Potential Genetic Contributions of the Central Nervous System to a Predisposition to Elite Athletic Traits: State-of-the-Art and Future Perspectives

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 371
Author(s):  
Hiroya Kitazawa ◽  
Kazuya Hasegawa ◽  
Daichi Aruga ◽  
Masashi Tanaka
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Exercise Performance ◽  
Future Research ◽  
Mental Performance ◽  
Research Directions ◽  
Genetic Technologies ◽  
The Central Nervous System ◽  
Future Research Directions ◽  
Genetic Contributions

Recent remarkable advances in genetic technologies have allowed for the identification of genetic factors potentially related to a predisposition to elite athletic performance. Most of these genetic variants seem to be implicated in musculoskeletal and cardiopulmonary functions. Conversely, it remains unclear whether functions of the central nervous system (CNS) genetically contribute to elite athletic traits, although the CNS plays critical roles in exercise performance. Accumulating evidence has highlighted the emerging implications of CNS-related genes in the modulation of brain activities, including mental performance and motor-related traits, thereby potentially contributing to high levels of exercise performance. In this review, recent advances are summarized, and future research directions are discussed in regard to CNS-related genes with potential roles in a predisposition to elite athletic traits.

scholarly journals Synapse development is regulated by microglial THIK-1 K+ channels

2021 ◽  
Vol 118 (42) ◽  
pp. e2106294118
Author(s):  
Pablo Izquierdo ◽  
Hiroko Shiina ◽  
Chanawee Hirunpattarasilp ◽  
Grace Gillis ◽  
David Attwell
Keyword(s):  
Neural Circuit ◽  
Brain Parenchyma ◽  
Glutamatergic Synapses ◽  
Microglial Phagocytosis ◽  
Disease States ◽  
Intracellular Ca ◽  
The Central Nervous System ◽  
Circuit Function ◽  
Dying Cells ◽  
The Brain

Microglia are the resident immune cells of the central nervous system. They constantly survey the brain parenchyma for redundant synapses, debris, or dying cells, which they remove through phagocytosis. Microglial ramification, motility, and cytokine release are regulated by tonically active THIK-1 K+ channels on the microglial plasma membrane. Here, we examined whether these channels also play a role in phagocytosis. Using pharmacological blockers and THIK-1 knockout (KO) mice, we found that a lack of THIK-1 activity approximately halved both microglial phagocytosis and marker levels for the lysosomes that degrade phagocytically removed material. These changes may reflect a decrease of intracellular [Ca2+]i activity, which was observed when THIK-1 activity was reduced, since buffering [Ca2+]i reduced phagocytosis. Less phagocytosis is expected to result in impaired pruning of synapses. In the hippocampus, mice lacking THIK-1 expression had an increased number of anatomically and electrophysiologically defined glutamatergic synapses during development. This resulted from an increased number of presynaptic terminals, caused by impaired removal by THIK-1 KO microglia. The dependence of synapse number on THIK-1 K+ channels, which control microglial surveillance and phagocytic ability, implies that changes in the THIK-1 expression level in disease states may contribute to altering neural circuit function.

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