The high affinity uptake system for excitatory amino acids in the brain
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2018, Brain ResearchCitation Excerpt :Excitotoxicity is one of the major disease mechanisms ascribed to contributing to the degeneration of motor neurons in ALS (Rothstein et al., 1991; Taylor et al., 2016) (Fig. 2), while less is known about excitotoxic mechanisms in FTD. One of the underlying mechanisms of excitotoxicity in ALS is the loss of glial glutamate transporters, which, under normal physiological conditions, are responsible for maintaining a tightly controlled glutamate homeostasis in the synaptic cleft, ensuring fast neuronal synaptic transmission (Danbolt et al., 1992; Danbolt, 1994; Danbolt et al., 1994). Rothstein and colleagues initially observed increased glutamate levels in ALS patient-derived cerebral spinal fluid and were then able to show selective loss of glutamate transporter EAAT2 in postmortem motor cortex brain tissue of ALS patients when compared to healthy control subjects (Rothstein et al., 1990; Rothstein et al., 1995).
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