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Excitatory amino acid transporter (EAAT (with specific isoforms such as EAAT1, EAAT2, etc.))

Target
EAAT (with specific isoforms such as EAAT1, EAAT2, etc.)
Molecular classification
Transporter, Neurotransmitter transporter, Solute carrier family protein
01

Overview

Excitatory amino acid transporters are a family of secondary active transporters that rapidly remove the neurotransmitter glutamate from the synaptic cleft after its release from presynaptic nerve terminals. They belong to the solute carrier family 1 (SLC1) and include several isoforms in mammals—EAAT1 through EAAT5—with distinct tissue distributions and physiological roles. These transporters are essential for maintaining low extracellular concentrations of glutamate in the central nervous system, thereby preventing excitotoxic neuronal damage while ensuring proper termination and modulation of synaptic signaling. Dysfunction or altered expression is implicated in various neurological diseases including ALS, episodic ataxia type 6, schizophrenia-related sensory gating deficits, and other neurodegenerative conditions. Pharmacologically relevant drugs can modulate their activity by either inhibiting their function directly or upregulating their expression to enhance neuroprotection. Some members also function as anion channels in addition to their role as transporters.

Other names
Glutamate transporterSolute carrier family 1 member (SLC1A)GLAST (for EAAT1)GLT-1 (for EAAT2)Glutamate aspartate transporter 1 (GLAST-1 for EAAT1)
02

Mechanism of action

Inhibition or upregulation alters extracellular glutamate clearance, affecting neurotransmission and neuroprotection

03

Biological functions

Regulation of extracellular glutamate concentrationTermination of glutamatergic synaptic transmissionPrevention of glutamate excitotoxicityModulation of synaptic responses and information processing in the CNS
04

Disease associations

Neurodegenerative disease (e.g., amyotrophic lateral sclerosis/ALS)Episodic ataxia type 6Schizophrenia/sensory gating deficitsOsteoarthritisOther CNS pathologies related to excitotoxicity
05

Safety considerations

Potential for impaired neurotransmission if over-inhibited or under-expressed, leading to excitotoxicity or neurological dysfunctions such as ataxia or ALS-like symptoms
06

Interacting drugs

Riluzole (upregulates EAAT2)

2 more in the full profile.

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