Chapter 22: Hepatic encephalopathy: a disorder in glial-neuronal communication
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Hyperammonemia in Hepatic Encephalopathy
2018, Journal of Clinical and Experimental HepatologyCitation Excerpt :Astrocytes are also involved in synapse formation during development, as well as in their maintenance in adults.105 Further, astrocytic dysfunction in CHE has been postulated to also to largely contribute to the neurobehavioral abnormalities associated with CHE.106–111 Among their many biological roles, astrocytes are also important for neuronal development, synaptic transmission, homeostasis, and neuroprotection.105
Reactive Nitrogen and Oxygen Species in Hepatic Encephalopathy
2017, Liver Pathophysiology: Therapies and AntioxidantsNeuroinflammation in hepatic encephalopathy: Mechanistic aspects
2015, Journal of Clinical and Experimental HepatologyThe role of glia in stress: Polyamines and brain disorders
2014, Psychiatric Clinics of North AmericaCitation Excerpt :Failure of synaptic transmission64,65 and vasodilation66,67 has been ascribed to the malfunction of perisynaptic and perivascular astrocytes, respectively. Neuronal damage is evident after glial depletion in hepatic encephalopathy,68 and neuronal degeneration can occur after apoptosis of glial cells.69 It has long been accepted that glia provide a support function to neurons by buffering extracellular K+ and glutamate.70–74
Role of cerebral endothelial cells in the astrocyte swelling and brain edema associated with acute hepatic encephalopathy
2012, NeuroscienceCitation Excerpt :All animal procedures followed guidelines established by the National Institute of Health Guide for the Care and Use of Laboratory Animals and were approved by our Institutional Animal Care and Use Committee (IACUC). The use of ammonia-treated cultured astrocytes as a model for hepatic encephalopathy is highly appropriate since substantial evidence invokes the role of ammonia in the pathogenesis of hepatic encephalopathy (Albrecht and Jones, 1999; Hazell and Butterworth, 1999), and astrocytes are the principal cells affected in this condition (Norenberg, 1981, 1998; Norenberg et al., 1992). Moreover, many of the findings occurring in hepatic encephalopathy in vivo are also observed in these cultures, including characteristic morphologic changes, cell swelling, defects in glutamate transport, up-regulation of the peripheral benzodiazepine receptor (recently renamed the 18-kDa translocator protein), reduction in levels of GFAP and myo-inositol, disturbance in energy metabolism, and evidence of oxidative/nitrosative stress (for review, see Norenberg et al., 2009).
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