Electrogenic-coupled (Na+ and K+) glutamate transporters in nerve terminals and glial cells are essential for maintaining subtoxic levels of extracellular excitatory amino acid neurotransmitters (e.g. glutamate and aspartate). They are also important for modifying synaptic transmission through the cotransport of ions and neurotransmitters. Excitatory amino acid transporter 2 (EAAT2) has 8 α-helical transmembrane domains and two reentrant pore-loop-like structures whose conformation is altered during ion neurotransmitter transport. EAAT2 is primarily expressed in astrocytes in adult brain and spinal cord, however it is also found in axons during fetal development. Mice deficient in EAAT2 exhibit lethal epileptic seizures with destruction of hippocampal neurons and an increased susceptibility to cold-induced cortical injury. Such defects in glutamine transporters have also been implicated in stroke, brain trauma, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease. Thus, glutamine transporters, such as EAAT2, are critical for prevention of neurotoxic brain injury and may regulate glutamatergic synaptic transmission.
This antibody is routinely tested by western blot analysis. Other applications were tested at BD Biosciences Pharmingen during antibody development only or reported in the literature.