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Mechanobiology in Health and Disease in the Central Nervous System
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Theresa A. Ulrich, Sanjay Kumar
The idea that astrocytes may be ideally situated to sense and resist mechanical disruption in the brain through their unique scaffold architecture is not new; in fact, it has been over two decades since Alen Mathewson and Martin Berry first hypothesized that “architectural disruption” in the brain may be responsible for the phenomenon of astrocyte activation [108]. This activation, also referred to as reactive gliosis or astrogliosis, involves both astrocyte hypertrophy (abnormal enlargement of cell size) and hyperplasia (increase in cell number) in response to CNS pathologies ranging from neurodegenerative diseases to direct trauma, and often results in the formation of a glial scar [109]. Because astrocytes function as a syncytium of interconnected cells, mechanical deformation in one area of the brain due to primary stress (e.g., the mass effect of a tumor or direct stress due to trauma) or secondary stress (e.g., increasing pressure due to edema, the buildup of fluid following tissue insult) could quickly be biochemically and mechanically communicated to distant astrocytes, allowing rapid induction of reactive gliosis and other host response mechanisms.
Mapping the Injured Brain
Published in Yu Chen, Babak Kateb, Neurophotonics and Brain Mapping, 2017
Chandler Sours, Jiachen Zhuo, Rao P. Gullapalli
Much of what has been learned regarding structural alterations following trauma have come from experimental models of TBI in rodent studies. Pathophysiology results from these studies suggest initially the axons swell up in response to injury due to the loss of integrity of ionic transport channels located on the axon. While some swelling resolves, extensive unresolved swelling often results in broken axons with terminal axon bulbs. Accompanying damage may also involve loss of the integrity of the myelin sheath known as demyelination. This demyelination often progresses over time which results in reduced axonal integrity in the chronic stages of injury. In addition to direct axonal damage, the injury also results in a transient increase in numbers of astrocytes and microglial cells (Chen et al., 2003). The atypical increase in the number of astrocytes in a region due to the death of nearby neurons is referred to as astrogliosis. Reactive astrogliosis are believed to play essential roles in preserving healthy neurons and minimizing inflammation within the surrounding brain tissue (Myer et al., 2006).
The therapeutic effect of nano-zinc on the optic nerve of offspring rats and their mothers treated with lipopolysaccharides
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Eman Mohammed Emara, Hassan Ih El-Sayyad, Amr M Mowafy, Heba a El-Ghaweet
The optic nerve (cranial nerve II) is a central nervous system (CNS) tract that passes through the optic canal to leave the orbit. It is made up of the retinal ganglion cells (RGCs) axons. It allows vision by transmitting neural impulses from the retina to the brain. It is divided into four sections: the intraocular nerve head, the intraorbital, the intracanalicular and the intracranial [6]. The types of glial cells in the optic nerve are oligodendrocytes, astrocytes and microglia. Oligodendrocytes are responsible for producing the myelin sheaths that protect the CNS axons and contact nodes of Ranvier as well as they are the locations where action potentials are propagated and axonal integrity. Astrocytes are responsible for numerous physiological and pathological activities such as potassium homeostasis and metabolism as well as reactive astrogliosis in response to CNS trauma. Microglia are immune cells in CNS and have a significant impact on inflammation and infections [7].
Reactive astrogliosis in the dentate gyrus of mice exposed to active volcanic environments
Published in Journal of Toxicology and Environmental Health, Part A, 2021
A. Navarro, M. García, A.S. Rodrigues, P.V. Garcia, R. Camarinho, Y. Segovia
Data demonstrated the presence of reactive astrogliosis in the DG of the hippocampus attributed to living in an active volcanic environment. The hippocampus has been considered a target structure for neurotoxic agents as abuse of drugs, neuroactive virus, or environmental pollutants (Harry and D’Hellencourt 2003; Walsh and Emerich 1988). It is of interest that the DG seems to be affected by a chronic exposure to volcanogenic air pollution (Navarro-Sempere et al. 2020). Consequently, it is an ideal structure to examine different astroglial dysfunction processes. Further, it is well established that astrocytes are highly differentiated cells that contribute to the proper functioning of a healthy CNS, in addition to responding to damage and disease through a process termed reactive astrogliosis (Sofroniew 2009). Pekny, Wilhelmsson, and Pekna (2014) identified two prominent hallmarks that are produced in reactive astrogliosis: (1) hypertrophy of the astrocytic branches and (2) upregulation of the intermediate filament proteins, especially GFAP. The animals captured in Furnas village displayed a significant rise in the number of GFAP+ astrocytes and branches morphological changes compared to mice caught in the control area, Rabo de Peixe, in which astrocytes exhibited normal morphology.