title: [Astrocytes--anonymous cells in the brain, participating in neurasthenic symptoms].
abstract: During rehabilitation after brain damage due to stroke or trauma, or after meningitis, patients often suffer from mental fatigue and decreased capacity for concentration and learning. We hypothesize that one pathogenic cause of these symptoms could be a failure on the part of astroglia to remove glutamate and K+ from synaptic regions during glutamatergic transmission. As astroglial support of neuronal glutamate transmission has been shown to be of utmost importance, such an astroglial failing might lead to a decreased signal-to-noise ratio in glutamatergic neurotransmission, especially when the transmission is intense for a considerable time period. Three aspects of astroglial failing are focused upon: decreased capacity of the astroglial glutamate transporters, depolarization of the astroglial network, and uncoupling of the gap junction coupled astroglial network. It has been shown that several neuroactive substances, present within the nervous system even long after damage or infection, influence upon these three astroglial properties.
authors.affiliation: Institutionen för klinisk neurovetenskap, Göteborgs universitet.
authors.forename: L
authors.initials: L
authors.lastname: Rönnbäck
authors.forename: T
authors.initials: T
authors.lastname: Olsson
authors.forename: E
authors.initials: E
authors.lastname: Hansson
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000502:physiology*; D002450:Cell Communication; D015673:Fatigue Syndrome, Chronic / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D017629:Gap Junctions / Q000378:metabolism / Q000502:physiology; D005971:Glutamates / Q000378:metabolism; D006801:Humans; D008488:Medical Illustration; D009440:Neurasthenia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D011188:Potassium / Q000378:metabolism; D009435:Synaptic Transmission
chemical_list: D005971:Glutamates; D011188:Potassium