In this special issue of Nature Neuroscience, we shine a spotlight on glia. Research into glia has become one of the most exciting and dynamic subfields of neuroscience, yet there is still much to be discovered about the diverse forms and functions of these cells.

Neuroscience has traditionally been a neuron-centric field. We have extensively studied how neurons assemble into circuits, communicate with each other, sense and respond to their environments, and change with time and experience. Within this neuron-centric framing, the nonneuronal cells of the nervous system, glia, were regarded as passive support cells (the term ‘glia’ derives from the Greek word for glue) and have received less attention.

Glia is a blanket term that refers to several very different cell-types: astrocytes, microglia and oligodendrocytes (as well as their antecedents, oligodendrocyte precursor cells). According to the canonical view one might read in a textbook, astrocytes have a role in regulating brain metabolism, taking up and releasing neurotransmitters, and establishing the blood–brain barrier. Microglia are innate immune cells of the brain that clear debris and respond to inflammatory stimuli. Oligodendrocytes wrap around axons, and form myelin sheaths that are critical for proper conduction of action potentials.

But as research into glia has deepened and expanded, we have learned that these cells are much more dynamic and multifaceted than had previously been understood. Glia contain multitudes. Single-cell and spatial transcriptomics studies have revealed that, as with neurons, glia comprise a diverse array of cellular subtypes and states. Microglial processes are in constant motion, surveilling and responding to their environment. Astrocytes have been shown to be involved in perhaps surprisingly complex aspects of memory and other cognitive functions. Myelin undergoes experience-dependent changes that contribute to learning and plasticity. Microglia, astrocytes and oligodendrocyte precursor cells have all been shown to contribute to synaptic pruning in various contexts. And multiple glial cell types have been implicated in a wide array of neurodegenerative and psychiatric diseases.

As the editors of Nature Neuroscience, we have been exhilarated by the pace of discoveries in this area and are delighted to showcase some of this transformative work in our pages. This month’s issue represents a celebration of glia from start to finish. We begin by highlighting some exciting papers about glia that have been published in other journals in recent weeks. We share conversations with established leaders and emerging voices in the field, Lucas Cheadle, Sonia Mayoral, Beth Stevens and Andrea Volterra. A Review from Lindsay Osso and Ethan Hughes challenges the dogmatic view of myelin as static and illuminates what is known about its renewal and remodeling.

We also present primary research papers that reflect the breadth of the glial research field. Tewari et al. describe how astrocytic regulation of synapses depends on perineuronal nets, and O’Shea et al. characterize border-forming wound-repair astrocytes that emerge following spinal cord injury or stroke. Foerster et al. demonstrate a role for oligodendrocyte heterogeneity — specifically cells of dorsal versus ventral origin — in brain development, and we learn about roles for oligodendrocyte lineage cells in diseases that have mostly been thought of as involving neurons: neurofibromatosis type 1 and prion-induced neurodegeneration. Three papers examine interactions between microglia and other glial cell types: Kedia, Ji and colleagues reveal how CD8+ T cells trigger microglia to damage myelin in a mouse model of Alzheimer’s disease; Chen, Luan, Liu and colleagues describe how brain injury causes astrocytic ATP release (an ‘inflare’) that in turn signals to microglia; and Huang, Wang and colleagues examine how plexin-B1 expressed in periplaque reactive astrocytes in a mouse model of Alzheimer’s disease restricts access of microglia to amyloid plaques. Brown et al. even describe some circuit maturation processes that do not require microglia. And, rest assured, we have some compelling papers for our neuron-loving readers, too.

Despite the recent acceleration of discoveries about glia, many important questions remain unanswered. How exactly do glia regulate synapses, including synaptogenesis, synaptic transmission, pruning and plasticity? How do glial cells acquire their complex morphologies, and what are the functions of their elaborate processes? How do glia interact with immune and vascular cells? How do we make sense of the vast diversity of glial subtypes, and which of these types or states are beneficial versus deleterious in brain disease? How might the various glial subtypes contribute to neural coding and function? What sets apart human glia from those in other organisms? We look forward to seeing how the field will answer these and other questions in the years to come.