EAAT4

EAAT4 is a human aspartate/glutamate transporter predominantly expressed in the cerebellum and functions as a ligand-gated chloride channel^[1]. Mechanistically, EAAT4 localizes mainly to Purkinje cell dendrites, forms parasagittal cerebellar compartments, and concentrates near synapses in dendritic membranes facing astroglia^[2][3]. Compared with EAAT1-EAAT3, EAAT4 shows high-affinity, low-capacity glutamate transport, slower kinetics, and distinct voltage dependence, supporting a role in binding residual extracellular glutamate rather than rapid bulk uptake^[4]. In cerebellar models, EAAT4 shapes mGluR signaling, controls synaptic plasticity, and limits transmitter diffusion from climbing fibers^[5][6]. Loss-of-function studies show that EAAT4 loss alters Purkinje cell firing and survival, distinguishing neuronal EAAT4 from glial GLAST/EAAT1 in cerebellar disease-relevant mechanisms^[7]. For experimental applications, TBOA inhibits EAAT4 currents and can help test transporter-dependent glutamate uptake and anion conductance in heterologous or cerebellar preparations^[4].- EAAT4 links glutamate clearance, chloride conductance, and Purkinje cell compartmental signaling.- EAAT4 differs from EAAT1-EAAT3 by slower, high-affinity, low-capacity transport kinetics.- TBOA-based inhibition supports functional testing of EAAT4-dependent glutamate uptake mechanisms.