RESUMO
Microglia are long-lived resident macrophages of the brain with diverse roles that span development, adulthood, and aging. Once thought to be a relatively homogeneous population, there is a growing recognition that microglia are highly specialized to suit their specific brain region. Cerebellar microglia represent an example of such specialization, exhibiting a dynamical, transcriptional, and immunological profile that differs from that of other microglial populations. Here we review the evidence that cerebellar microglia shape the cerebellar environment and are in turn shaped by it. We examine the roles microglia play in cerebellar function, development, and aging. The emerging findings on cerebellar microglia may also provide insights into disease processes involving cerebellar dysfunction.
Assuntos
Envelhecimento , Microglia , Adulto , Encéfalo , Cerebelo , HumanosRESUMO
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
RESUMO
Microglia are the brain's resident innate immune cells and also have a role in synaptic plasticity. Microglial processes continuously survey the brain parenchyma, interact with synaptic elements and maintain tissue homeostasis. However, the mechanisms that control surveillance and its role in synaptic plasticity are poorly understood. Microglial dynamics in vivo have been primarily studied in anesthetized animals. Here we report that microglial surveillance and injury response are reduced in awake mice as compared to anesthetized mice, suggesting that arousal state modulates microglial function. Pharmacologic stimulation of ß2-adrenergic receptors recapitulated these observations and disrupted experience-dependent plasticity, and these effects required the presence of ß2-adrenergic receptors in microglia. These results indicate that microglial roles in surveillance and synaptic plasticity in the mouse brain are modulated by noradrenergic tone fluctuations between arousal states and emphasize the need to understand the effect of disruptions of adrenergic signaling in neurodevelopment and neuropathology.