Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes. In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar.
The process of gliosis involves a series of cellular and molecular events that occur over several days. Typically, the first response to injury is the migration of macrophages and local microglia to the injury site. This process, which constitutes a form of gliosis known as microgliosis, begins within hours of the initial CNS injury. Later, after 3–5 days, oligodendrocyte precursor cells are also recruited to the site and may contribute to remyelination. The final component of gliosis is astrogliosis, the proliferation of surrounding astrocytes, which are the main constituents of the glial scar.
Gliosis has historically been given a negative connotation due to its appearance in many CNS diseases and the inhibition of axonal regeneration caused by glial scar formation. However, gliosis has been shown to have both beneficial and detrimental effects, and the balance between these is due to a complex array of factors and molecular signaling mechanisms, which affect the reaction of all glial cell types.
Astrogliosis
Reactive astrogliosis is the most common form of gliosis and involves the proliferation of astrocytes, a type of glial cell responsible for maintaining extracellular ion and neurotransmitter concentrations, modulating synapse function, and forming the blood–brain barrier. Like other forms of gliosis, astrogliosis accompanies traumatic brain injury as well as many neuropathologies, ranging from amyotrophic lateral sclerosis to fatal familial insomnia. Although the mechanisms which lead to astrogliosis are not fully understood, neuronal injury is well understood to cause astrocyte proliferation, and astrogliosis has long been used as an index for neuronal damage.
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Radial glial cells, or radial glial progenitor cells (RGPs), are bipolar-shaped progenitor cells that are responsible for producing all of the neurons in the cerebral cortex. RGPs also produce certain lineages of glia, including astrocytes and oligodendrocytes. Their cell bodies (somata) reside in the embryonic ventricular zone, which lies next to the developing ventricular system. During development, newborn neurons use radial glia as scaffolds, traveling along the radial glial fibers in order to reach their final destinations.
Astrogliosis (also known as astrocytosis or referred to as reactive astrogliosis) is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system (CNS) trauma, infection, ischemia, stroke, autoimmune responses or neurodegenerative disease. In healthy neural tissue, astrocytes play critical roles in energy provision, regulation of blood flow, homeostasis of extracellular fluid, homeostasis of ions and transmitters, regulation of synapse function and synaptic remodeling.
Glial fibrillary acidic protein (GFAP) is a protein that is encoded by the GFAP gene in humans. It is a type III intermediate filament (IF) protein that is expressed by numerous cell types of the central nervous system (CNS), including astrocytes and ependymal cells during development. GFAP has also been found to be expressed in glomeruli and peritubular fibroblasts taken from rat kidneys, Leydig cells of the testis in both hamsters and humans, human keratinocytes, human osteocytes and chondrocytes and stellate cells of the pancreas and liver in rats.
The goal of the course is to guide students through the essential aspects of molecular neuroscience and neurodegenerative diseases. The student will gain the ability to dissect the molecular basis of
Explores the structure and function of glial cells in the nervous system, including their roles in myelination, synaptic transmission, and memory formation.
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