Abstract
Glutamate is the major excitatory neurotransmitter and plays important roles in the physiology of the mammalian central nervous system. In spite of its importance as a neurotransmitter, too much glutamate is toxic to neurons. Removal of glutamate from the extracellular space is critical for keeping the extracellular glutamate concentration below toxic level, and is mediated by GLT1 (EAAT2) and GLAST (EAAT1) , which are primarily expressed by astrocytes. Rare loss-of-function variants and down-regulation of GLT1 and GLAST have been reported in psychiatric disorders. In this review, we demonstrate that various kinds of GLT1 and/or GLAST knockout mice recapitulate many aspects of the developmental defects and behavioral abnormalities seen in human patients with major mental illnesses including schizophrenia and depression.
