Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1.
Journal:
Science 1997 JunAuthors:
Tanaka K, Watase K, Manabe T, Yamada K, Watanabe M, Takahashi K, Iwama H, Nishikawa T, Ichihara N, Kikuchi T, Okuyama S, Kawashima N, Hori S, Takimoto M, Wada K
Abstract
Extracellular levels of the excitatory neurotransmitter glutamate in the nervous system are maintained by transporters that actively remove glutamate from the extracellular space. Homozygous mice deficient in GLT-1, a widely distributed astrocytic glutamate transporter, show lethal spontaneous seizures and increased susceptibility to acute cortical injury. These effects can be attributed to elevated levels of residual glutamate in the brains of these mice.
Mesh Headings:
ATP-Binding Cassette Transporters, Amino Acid Transport System X-AG, Animals, Biological Transport, Brain, Brain Injuries, Electroencephalography, Epilepsy, Gene Targeting, Glutamic Acid, Hippocampus, Mice, Mice, Inbred C57BL, Nerve Degeneration, Pyramidal Cells, Synapses, Synaptic Transmission