The EAATs are membrane-bound secondary transporters that superficially resemble ion channels.
[4] There are two general classes of glutamate transporters, those that are dependent on an electrochemical gradient of sodium ions (the EAATs) and those that are not (VGLUTs and xCT).
Na+-dependent EAATs are also dependent on transmembrane K+ and H+concentration gradients, and so are also known as 'sodium and potassium coupled glutamate transporters'.
Subtypes EAAT1-2 are found in membranes of glial cells[13] (astrocytes, microglia, and oligodendrocytes).
[7][12] The EAAT3-4 subtypes are exclusively neuronal, and are expressed in axon terminals,[8] cell bodies, and dendrites.
VGLUTs are dependent on the proton gradient that exists in the secretory system (vesicles being more acidic than the cytosol).
Certainly, no significant change was found in aggression and depression-like behaviors, but in contrast, the loss of VGluT3 resulted in a specific anxiety-related phenotype.
In this case, Vesicular glutamate transporter 3 (VGluT3), have been implicated in mechanical hypersensitivity after inflammation, but their role in neuropathic pain still remains under debate.
After the elevator motion brings the substrate to the IC side of the membrane, EAAT adopts the inward facing (IF, closed) state in which the transport domain is lowered, but the HP2 gate is still closed with the glutamate still bound to the transporter.
In fact, their activity may also actually be reversed due to inadequate amounts of adenosine triphosphate to power ATPase pumps, resulting in the loss of the electrochemical ion gradient.
[28] Also, degeneration of motor neurons in the disease amyotrophic lateral sclerosis has been linked to loss of EAAT2 from patients' brains and spinal cords.