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The P2Y12 receptor regulates microglial activation by extracellular nucleotides. ATP release during seizures-a critical evaluation of the evidence. Dopamine-evoked synaptic regulation in the nucleus accumbens requires astrocyte activity. Neurobiology: astrocytic purinergic signaling coordinates synaptic networks. Vesicular release of ATP at central synapses. Acute focal seizures start as local synchronizations of neuronal ensembles.
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Molecular diversity and specializations among the cells of the adult mouse brain. CSF1R ligands IL-34 and CSF1 are differentially required for microglia development and maintenance in white and gray matter brain regions. CSF-1 controls cerebellar microglia and is required for motor function and social interaction. Emerging roles for CSF-1 receptor and its ligands in the nervous system. The role of dopamine signaling in epileptogenesis. Colony-stimulating factor 1 receptor signaling is necessary for microglia viability, unmasking a microglia progenitor cell in the adult brain. Noradrenergic signaling in the wakeful state inhibits microglial surveillance and synaptic plasticity in the mouse visual cortex. Neuronal network activity controls microglial process surveillance in awake mice via norepinephrine signaling. Microglial ramification, surveillance, and interleukin-1β release are regulated by the two-pore domain K + channel THIK-1. Nanoscale surveillance of the brain by microglia via cAMP-regulated filopodia. Microglia monitor and protect neuronal function through specialized somatic purinergic junctions. Microglial P2Y12 receptor regulates ventral hippocampal CA1 neuronal excitability and innate fear in mice. Resting microglia directly monitor the functional state of synapses in vivo and determine the fate of ischemic terminals. Microglial contact prevents excess depolarization and rescues neurons from excitotoxicity. Microglia enhance synapse activity to promote local network synchronization. Neuronal hyperactivity recruits microglial processes via neuronal NMDA receptors and microglial P2Y12 receptors after status epilepticus. Reciprocal regulation between resting microglial dynamics and neuronal activity in vivo. A microglia-cytokine axis to modulate synaptic connectivity and function. Our findings suggest that this microglia-driven negative feedback mechanism operates similarly to inhibitory neurons and is essential for protecting the brain from excessive activation in health and disease.
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Microglial sensing of ATP, the ensuing microglia-dependent production of adenosine, and the adenosine-mediated suppression of neuronal responses via the adenosine receptor A 1R are essential for the regulation of neuronal activity and animal behaviour. ATP triggers the recruitment of microglial protrusions and is converted by the microglial ATP/ADP hydrolysing ectoenzyme CD39 into AMP AMP is then converted into adenosine by CD73, which is expressed on microglia as well as other brain cells. Suppression of neuronal activation by microglia occurs in a highly region-specific fashion and depends on the ability of microglia to sense and catabolize extracellular ATP, which is released upon neuronal activation by neurons and astrocytes. Microglia respond to neuronal activation by suppressing neuronal activity, and ablation of microglia amplifies and synchronizes the activity of neurons, leading to seizures. Here we show that microglia are also critical modulators of neuronal activity and associated behavioural responses in mice. Microglia, the brain’s resident macrophages, help to regulate brain function by removing dying neurons, pruning non-functional synapses, and producing ligands that support neuronal survival 1. Nature volume 586, pages 417–423 ( 2020) Cite this article Negative feedback control of neuronal activity by microglia