title: Homeostatic regulation of glutamate release in response to depolarization.
abstract: Proper nervous system function requires a balance between excitation and inhibition. Systems of homeostasis may have evolved in neurons to help maintain or restore balance between excitation and inhibition, presumably because excessive excitation can cause dysfunction and cell death. This article reviews evidence for homeostatic mechanisms within the hippocampus that lead to differential regulation of glutamate and gamma-aminobutyric acid release in response to conditions of excess depolarization. We recently found differential effects on glutamate release at the level of action potential coupling to transmitter release, vesicular release probability, and vesicle availability. Such differential regulation may help to prevent excitotoxicity and runaway excitation.
authors.affiliation: Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA.
authors.forename: Krista L
authors.initials: KL
authors.lastname: Moulder
authors.forename: Julian P
authors.initials: JP
authors.lastname: Meeks
authors.forename: Steven
authors.initials: S
authors.lastname: Mennerick
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D018698:Glutamic Acid / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism*; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D009433:Neural Inhibition / Q000502:physiology; D017729:Presynaptic Terminals / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013572:Synaptic Vesicles / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D007473:Ion Channels; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid