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The evolution of the nervous system progressed through cellular diversification and specialization of functions. Conceptually, the nervous system is composed of electrically excitable neuronal networks connected by chemical synapses and nonexcitable glial cells that provide for homeostasis and defense. The evolution of neuroglia began with the emergence of the centralized nervous system and proceeded through a continuous increase in their complexity. In the primate brain, especially in the brain of humans, the astrocyte lineage is exceedingly complex, with the emergence of new types of astroglial cells possibly involved in interlayer communication and integration. [ABSTRACT FROM AUTHOR]

Synaptic plasticity is closely related to the development and repair after injury in the nervous system. Glial cells maintain close communication with neurons through energy transportation and signal transduction, which is an important way to promote synaptic plasticity. Astrocytes are closely related to synapses in morphology and function, and are an important factor in regulating synaptic plasticity. Microglia carry out two-way information interaction with synapses, which is a key regulator of synaptic plasticity during development and adulthood. Oligodendrocytes participate in the formation of myelin sheaths, provide metabolic substrates for synaptic transmission, which is a potential force to promote synaptic plasticity. This paper reviews the research progress on the relationship between astrocytes, microglia, oligodendrocytes and synaptic plasticity, in order to provide the reference for further understanding the relationship between glial cells and synaptic plasticity. [ABSTRACT FROM AUTHOR]

Circuit reorganization after injury was studied in a cerebellar culture model. When cerebellar cultures derived from newborn mice were exposed at explantation to a preparation of cytosine arabinoside that destroyed granule cells and oligodendrocytes and compromised astrocytes, Purkinje cells surviving in greater than usual numbers were unensheathed by astrocytic processes and received twice the control number of inhibitory axosomatic synapses. Purkinje cell axon collaterals sprouted and many of their terminals formed heterotypical synapses with other Purkinje cell dendritic spines. The resulting circuit reorganization preserved inhibition in the cerebellar cortex. Following this reorganization, replacement of the missing granule cells and glia was followed by a restitution of the normal circuitry. Most of these developmental and reconstructive changes were not dependent on neuronal activity, the major exception being inhibitory synaptogenesis. The full complement of inhibitory synapses did not develop in the absence of neuronal activity, which could be mitigated by application of exogenous TrkB receptor ligands. Inhibitory synaptogenesis could also be promoted by activity-induced release of endogenous TrkB receptor ligands or by antibody activation of the TrkB receptor. [ABSTRACT FROM AUTHOR]

Highlights: [•] Origins and differentiation of cerebellar astrocytes and their lineage relationships with other cerebellar types. [•] Role of radial glia and Bergmann glia in cerebellar corticogenesis. [•] Specific role of astrocytes and Bergmann glia in the function of cerebellar circuits. [•] Origins and differentiation of cerebellar oligodendrocytes and their lineage relationships with other cerebellar types. [•] Functional interactions between oligodendrocyte progenitors and neurons in the adult cerebellum. [ABSTRACT FROM AUTHOR]

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease in which motor neurons throughout the brain and spinal cord progressively degenerate resulting in muscle atrophy, paralysis and death. Recent studies using animal models of ALS implicate multiple cell-types (e.g., astrocytes and microglia) in ALS pathogenesis in the spinal motor systems. To ascertain cellular vulnerability and cell-type specific mechanisms of ALS in the brainstem that orchestrates oral-motor functions, we conducted parallel single cell RNA sequencing (scRNA-seq) analysis using the high-throughput Drop-seq method. We isolated 1894 and 3199 cells from the brainstem of wildtype and mutant SOD1 symptomatic mice respectively, at postnatal day 100. We recovered major known cell types and neuronal subpopulations, such as interneurons and motor neurons, and trigeminal ganglion (TG) peripheral sensory neurons, as well as, previously uncharacterized interneuron subtypes. We found that the majority of the cell types displayed transcriptomic alterations in ALS mice. Differentially expressed genes (DEGs) of individual cell populations revealed cell-type specific alterations in numerous pathways, including previously known ALS pathways such as inflammation (in microglia), stress response (ependymal and an uncharacterized cell population), neurogenesis (astrocytes, oligodendrocytes, neurons), synapse organization and transmission (microglia, oligodendrocyte precursor cells, and neuronal subtypes), and mitochondrial function (uncharacterized cell populations). Other cell-type specific processes altered in SOD1 mutant brainstem include those from motor neurons (axon regeneration, voltage-gated sodium and potassium channels underlying excitability, potassium ion transport), trigeminal sensory neurons (detection of temperature stimulus involved in sensory perception), and cellular response to toxic substances (uncharacterized cell populations). DEGs consistently altered across cell types (e.g., Malat1), as well as cell-type specific DEGs, were identified. Importantly, DEGs from various cell types overlapped with known ALS genes from the literature and with top hits from an existing human ALS genome-wide association study (GWAS), implicating the potential cell types in which the ALS genes function with ALS pathogenesis. Our molecular investigation at single cell resolution provides comprehensive insights into the cell types, genes and pathways altered in the brainstem in a widely used ALS mouse model. • Conducted single cell RNA sequencing of brainstem of wildtype and mutant SOD1 mice. • Uncovered major known cell types and previously uncharacterized neuron subtypes. • Identified genes and pathways altered in individual cell types in mutant brainstem. • Uncovered genes consistently altered across cell types or cell-type specific genes. • Genes/pathways altered in the SOD1 model overlapped with known human ALS genes. [ABSTRACT FROM AUTHOR]