Antibiotics rescue neurons from glutamate attack.
L-glutamate is the major excitatory neurotransmitter in the brain and is responsible for normal brain function. However, high glutamate exposure triggers neuronal death, a process known as excitotoxicity. Excitotoxicity is associated with acute and chronic neurodegenerative diseases. Treating excitotoxicity using glutamate-receptor antagonists has not proven clinically viable, necessitating more sophisticated approaches. Rothstein and colleagues discovered that beta-lactam antibiotics protect neurons from excitotoxicity by increasing the number of glutamate transporters, which have a key role in clearing glutamate from the extracellular space. The design of compounds capable of modulating glutamate uptake represents a novel strategy for the treatment of neurodegenerative diseases.
Tanaka
Kohichi
K
Laboratory of Molecular Neuroscience, School of Biomedical Science and Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-Ku, Tokyo 113-8510, Japan. tanaka.aud@mri.tmd.ac.jp
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D018698:Glutamic Acid / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D019636:Neurodegenerative Diseases / Q000473:pathology; D009474:Neurons / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism
D000900:Anti-Bacterial Agents; D018377:Neurotransmitter Agents; D018698:Glutamic Acid