Sodium-dependent excitatory amino acid transporter (EAAT)

Sodium-dependent excitatory amino acid transporters (EAATs) are a family of five plasma membrane proteins (EAAT1-5) that play a critical role in the central nervous system by clearing the excitatory neurotransmitter glutamate from the synaptic cleft (Danbolt, 2001) [1.3.1, 1.4.3]. This uptake mechanism is essential for terminating synaptic signaling and maintaining extracellular glutamate at sub-toxic levels, thereby preventing excitotoxicity and subsequent neuronal death (Campiani et al., 2003) [1.3.4]. EAAT1 and EAAT2 are primarily expressed in astrocytes, while EAAT3, EAAT4, and EAAT5 are predominantly neuronal (Wikipedia) [1.4.3]. Dysfunction or downregulation of these transporters, particularly EAAT2, is strongly associated with neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and epilepsy (NIH) [1.4.4]. Therapeutic strategies often focus on upregulating EAAT expression or activity to enhance glutamate clearance and provide neuroprotection (Bunch et al., 2009) [1.4.1]. Drugs like riluzole and ceftriaxone have been investigated for their ability to modulate EAAT2, though clinical applications are still being refined to address efficacy and delivery challenges (Rothstein et al., 2005) [1.4.1].

Other names

Excitatory amino acid transporterGlutamate transporterSolute carrier family 1GLASTGLT-1EAAC1Glutamate aspartate transporterExcitatory amino acid carrier 1

Transport activation, Transport upregulation, Transport inhibition