Neurons are the conducting cells of the nervous system. A typical neuron consists of a cell body, containing the nucleus and the surrounding cytoplasm ; several short radiating processes called dendrites ; and one long process called the axon , which terminates in twiglike branches and may have branches projecting along its course. In many ways, the cell body is similar to other types of cells.
The main function of these cells is to respond to any injuries or diseases in the CNS. When injury and disease are detected, the microglial are alerted and respond by moving to the injury site in order to either clear away any dead cells or to remove any harmful toxins or pathogens that may be present.
The cells are therefore especially important for maintaining the health of the CNS and are known as immune cells. Microglia also play a role in the development of the brain. Typically, far more synapses are created than are needed, when only the strongest and most important ones need to survive. Microglia directly contribute to removing synapses that are deemed as unnecessary, a process known as synaptic pruning.
Ependymal cells are located in the CNS that are column shaped and typically line up together to form a membrane. This membrane is called the ependyma, which is a thin membrane lining the spinal cord and ventricles of the brain. In the ventricles, these cells have tiny hairlike structures on them called cilia, which face the open space of the cavities they line. Cilia move in a coordinated pattern to encourage the directional flow of cerebrospinal fluid, which they also produce.
Cerebrospinal fluid works by allowing nutrients and other substances to reach the neurons as well as filtering out any harmful molecules. It also works as a cushion and shock absorber between the brain and the skull, as well as maintaining homeostasis of the brain such as regulating temperature.
A final type of glial in the CNS to discuss are radial glial. Radial glia is believed to be a type of stem cell, meaning they can generate other cells.
These cells are able to make neurons as well as other types of glial such as astrocytes and oligodendrocytes. Their role as stem cells, especially as being creators of neurons, makes them a target of interest for researchers who are looking into how to repair brain damage from injury and illness, or their role as the brain ages. Schwann cells work in a similar fashion to oligodendrocytes as they also produce myelin sheath for the axons of neurons, however, they are located in the PNS.
The plasma membrane of these Schwann cells spirals around the axons of neurons to form the fatty insulation that is required for faster transmission of electrical signals. Schwann cells can be either myelinating or non-myelinating. Whilst myelinating Schwann cells wrap around the axons of neurons, non-myelinating Schwann cells do not wrap around the axons, but they still provide support and cushioning to them.
Also, each Schwann cell form a single myelin sheath around an axon, whereas oligodendrocytes form myelin sheaths for multiple surrounding axons. In addition to insulating axons, Schwann cells are critical in response to axon damage within the PNS as they can help in regenerating these damaged axons. When any type of injury occurs, the Schwann cells are sent to the injury site to remove the dead cells.
The Schwann cells also have the capability to occupy the original space of the neurons and regenerate the fibers in such a way that they are able to return to their original target sites. The precentral gyrus is the anatomical location of the primary motor cortex , which is what this gyrus is commonly known as. The precentral gyrus is believed to contain the motor control for the torso, arms, hands, fingers, and head. Satellite cells small glia in the PNS that works by surrounding neurons in the sensory, sympathetic, and parasympathetic ganglia.
Ganglia are clusters of nerve selves within the autonomic nervous system as well as the sensory system. The autonomic nervous system regulates the internal organs, whilst the sensory system is important for our senses to work. These cells are thought to be similar to astrocytes in the CNS as they work in similar ways.
These cells also absorb harmful toxins so that they do not damage the neurons, as well as detecting and responding to injury and disease in the same way that microglia do. As previously discussed, glia cells are especially important for the overall functioning and support of neurons.
Therefore, if these cells are damaged in any way, can result in many complications, depending on the cells that have been damaged. Neurodegenerative disorders are particularly involved in glial damage. Development of monocytes, macrophages, and dendritic cells. Science , — Ghosh, A.
Targeted ablation of oligodendrocytes triggers axonal damage. Gowing, G. Ablation of proliferating microglia does not affect motor neuron degeneration in amyotrophic lateral sclerosis caused by mutant superoxide dismutase. Mouse model for ablation of proliferating microglia in acute CNS injuries.
Glia 53, — Grathwohl, S. Gritsch, S. Oligodendrocyte ablation triggers central pain independently of innate or adaptive immune responses in mice. Hanisch, U. Microglia: active sensor and versatile effector cells in the normal and pathologic brain.
Heppner, F. Experimental autoimmune encephalomyelitis repressed by microglial paralysis. Herculano-Houzel, S. Glia 62, — Hong, S. Complement and microglia mediate early synapse loss in Alzheimer mouse models. New insights on the role of microglia in synaptic pruning in health and disease. Honjo, T. Diphtheria toxin-dependent adenosine diphosphate ribosylation of aminoacyl transferase II and inhibition of protein synthesis.
Hughes, E. Oligodendrocyte progenitors balance growth with self-repulsion to achieve homeostasis in the adult brain. Irvine, K. A different regional response by mouse oligodendrocyte progenitor cells OPCs to high-dose X-irradiation has consequences for repopulating OPC-depleted normal tissue. Jaenisch, N. Downregulation of potassium chloride cotransporter KCC2 after transient focal cerebral ischemia. Stroke 41, e—e Johnson, I. De-intercalation of ethidium bromide and acridine orange by xanthine derivatives and their modulatory effect on anticancer agents: a study of DNA-directed toxicity enlightened by time correlated single photon counting.
Ji, K. Microglia actively regulate the number of functional synapses. Kalderon, N. Severed corticospinal axons recover electrophysiologic control of muscle activity after x-ray therapy in lesioned adult spinal cord. Karadottir, R. NMDA receptors are expressed in oligodendrocytes and activated in ischaemia.
Kaya, F. Live imaging of targeted cell ablation in Xenopus : a new model to study demyelination and repair. Kessaris, N. Competing waves of oligodendrocytes in the forebrain and postnatal elimination of an embryonic lineage. Kettenmann, H. Physiology of microglia. Oxford: Oxford University Press. Google Scholar. Khurgel, M. Selective ablation of astrocytes by intracerebral injections of alpha-aminoadipate.
Kigerl, K. Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. Kim, C. Brain trauma elicits non-canonical macrophage activation states. Neuroinflammation 13, Kim, S. Microglia in health and disease.
Kimelberg, H. Functions of mature mammalian astrocytes: a current view. Neuroscientist 16, 79— Functions of astrocytes and their potential as therapeutic targets.
Neurotherapeutics 7, — Kipp, M. The cuprizone animal model: new insights into an old story. Acta Neuropathol. Knox, R. Cancer Metastasis Rev. Kreutzberg, G. Microglia: a sensor for pathological events in the CNS. Trends Neurosci. Lalancette-Hebert, M. Selective ablation of proliferating microglial cells exacerbates ischemic injury in the brain. Lepore, A. Selective ablation of proliferating astrocytes does not affect disease outcome in either acute or chronic models of motor neuron degeneration.
Levine, J. The oligodendrocyte precursor cell in health and disease. Locatelli, G. Primary oligodendrocyte death does not elicit anti-CNS immunity. Loganovsky, K. Do low doses of ionizing radiation affect the human brain? Data Sci. May, D. Connexin47 protein phosphorylation and stability in oligodendrocytes depend on expression of Connexin43 protein in astrocytes. McKenzie, I. Motor skill learning requires active central myelination. Miron, V. M2 microglia and macrophages drive oligodendrocyte differentiation during CNS remyelination.
Mirrione, M. Microglial ablation and lipopolysaccharide preconditioning affects pilocarpine-induced seizures in mice. Myer, D. Essential protective roles of reactive astrocytes in traumatic brain injury. Brain , — Nave, K. Myelination and support of axonal integrity by glia.
Nimmerjahn, A. Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. Nishimura, R.
Induction of cell death by L-alpha-aminoadipic acid exposure in cultured rat astrocytes: relationship to protein synthesis. Neurotoxicology 21, — Oluich, L.
Targeted ablation of oligodendrocytes induces axonal pathology independent of overt demyelination. Parkhurst, C. Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor. Cell , — Pekny, M. Astrocyte reactivity and reactive astrogliosis: costs and benefits. Pignataro, G. Downregulation of hippocampal adenosine kinase after focal ischemia as potential endogenous neuroprotective mechanism.
Blood Flow Metab. Pineau, I. Brain Behav. Praet, J. Cellular and molecular neuropathology of the cuprizone mouse model: clinical relevance for multiple sclerosis. Psachoulia, K. Cell cycle dynamics of NG2 cells in the postnatal and ageing brain.
Neuron Glia Biol. Ransohoff, R. A polarizing question: do M1 and M2 microglia exist? Rhodes, K. The injury response of oligodendrocyte precursor cells is induced by platelets, macrophages and inflammation-associated cytokines. Neuroscience , 87— Rivers, L. Robel, S. The stem cell potential of glia: lessons from reactive gliosis.
Robins, S. Extensive regenerative plasticity among adult NG2-glia populations is exclusively based on self-renewal. Glia 61, — Rodriguez, J. Saffran, B. Putative gliotoxin, alpha-aminoadipic acid, fails to kill hippocampal astrocytes in vivo. Schneider, S. Decrease in newly generated oligodendrocytes leads to motor dysfunctions and changed myelin structures that can be rescued by transplanted cells. Glia 64, — Schreiner, B.
Astrocyte depletion impairs redox homeostasis and triggers neuronal loss in the adult CNS. Cell Rep. Silver, J. Central nervous system regenerative failure: role of oligodendrocytes, astrocytes, and microglia. Cold Spring Harb. Simon, C. Progenitors in the adult cerebral cortex: cell cycle properties and regulation by physiological stimuli and injury. Glia 59, — Sirko, S. Reactive glia in the injured brain acquire stem cell properties in response to sonic hedgehog.
Cell Stem Cell 12, — Skripuletz, T. Astrocytes regulate myelin clearance through recruitment of microglia during cuprizone-induced demyelination. Sofroniew, M. Astrocyte barriers to neurotoxic inflammation. Astrocytes: biology and pathology. Sun, W. Synaptic integration by NG2 cells. Szalay, G. Microglia protect against brain injury and their selective elimination dysregulates neuronal network activity after stroke. Takada, M. Fine structural changes in the rat brain after local injections of gliotoxin, alpha-aminoadipic acid.
Astroglial ablation prevents MPTP-induced nigrostriatal neuronal death. Brain Res. Takamiya, Y. Immunohistochemical studies on the proliferation of reactive astrocytes and the expression of cytoskeletal proteins following brain injury in rats. Thompson, M. Targeting cells of the myeloid lineage attenuates pain and disease progression in a prostate model of bone cancer. Pain , — Torres, L. Dynamic microglial modulation of spatial learning and social behavior.
Traka, M. Oligodendrocyte death results in immune-mediated CNS demyelination. Tsai, H. Regional astrocyte allocation regulates CNS synaptogenesis and repair. Depletion and repopulation of macrophages in spleen and liver of rat after intravenous treatment with liposome-encapsulated dichloromethylene diphosphonate. Cell Tissue Res. Vanderluit, J. Model for focal demyelination of the spinal dorsal columns of transgenic MBP-LacZ mice by phototargeted ablation of oligodendrocytes.
Varnum, M. Vasek, M. A complement-microglial axis drives synapse loss during virus-induced memory impairment. Transplantation reveals regional differences in oligodendrocyte differentiation in the adult brain. Voskuhl, R. Reactive astrocytes form scar-like perivascular barriers to leukocytes during adaptive immune inflammation of the CNS.
Waisman, A. Homeostasis of microglia in the adult brain: review of novel microglia depletion systems. Wang, A. Characteristics and functions of NG2 cells in normal brain and neuropathology. Wanner, I. Glial scar borders are formed by newly proliferated, elongated astrocytes that interact to corral inflammatory and fibrotic cells via STAT3-dependent mechanisms after spinal cord injury. Weisser, S. Generation and characterization of murine alternatively activated macrophages.
Methods Mol. Wilhelmsson, U. Absence of glial fibrillary acidic protein and vimentin prevents hypertrophy of astrocytic processes and improves post-traumatic regeneration. Wu, Y. Microglia: dynamic mediators of synapse development and plasticity. Xiao, L. Rapid production of new oligodendrocytes is required in the earliest stages of motor-skill learning.
Xu, H. Turnover of resident retinal microglia in the normal adult mouse. Yajima, K. Demyelination and remyelination in the rat central nervous system following ethidium bromide injection.
0コメント