Neuron-glial interaction during injury and edema of the CNS.
During injury and ischemia of the CNS mediator compounds are released or activated which cause secondary swelling and damage of nerve cells. Such mediators are glutamate, acidosis, free fatty acids, or high extracellular potassium. Glial homeostatic mechanisms are activated to prevent the secondary injury from these mediators. The glial clearance mechanisms have been studied in detail using in vitro systems allowing for a close control of the glial environment. Current evidence suggests glial swelling to occur together with glutamate uptake or in response to extracellular acidosis. Glial swelling, therefore, is rather the result of homeostatic mechanisms than an indication of glial demise.
Institute of Neurosurgical Pathophysiology, Johannes Gutenberg-Universität Mainz, Federal Republic of Germany.
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Kempski
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Volk
D000136:Acid-Base Equilibrium / Q000502:physiology; D000818:Animals; D001921:Brain / Q000503:physiopathology; D001929:Brain Edema / Q000503:physiopathology*; D001930:Brain Injuries / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology; D002450:Cell Communication / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D009457:Neuroglia / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000502:physiology
D018698:Glutamic Acid