Overactivity of<unk> s may result in inadequate synaptic<unk> amate and may be involved in schizophrenia and other mental illnesses. During injury processes such as ischemia and traumatic brain injury, the action of<unk> s may fail, leading to toxic buildup of<unk> amate. 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. Since the direction of<unk> amate transport depends on the ion gradient, these transporters release<unk> amate instead of removing it, which results in neurotoxicity due to overactivation of<unk> amate receptors. Loss of the Na+-dependent<unk>  EAAT2 is suspected to be associated with neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and ALS–parkinsonism dementia complex. Also, degeneration of motor neurons in the disease amyotrophic lateral sclerosis has been linked to loss of EAAT2 from patients' brains and spinal cords. Addiction to certain addictive drugs (e.g., cocaine, heroin, alcohol, and nicotine) is correlated with a persistent reduction in the expression of EAAT2 in the nucleus accumbens (NAcc); the reduced expression of EAAT2 in this region is implicated in addictive drug-seeking behavior. In particular, the long-term dysregulation of<unk> amate neurotransmission in the NAcc of addicts is associated with an increase in vulnerability to relapse after re-exposure to the addictive drug or its associated drug cues. Drugs which help to normalize the expression of EAAT2 in this region, such as N-acetylcysteine, have been proposed as an adjunct therapy for the treatment of addiction to cocaine, nicotine, alcohol, and other drugs.
Glutamate transporter
Norepinephrine transporter
Neurotransmitter transporter
Vesicular monoamine transporter
Vesicular monoamine transporter 1
Mechanosensitive channels
Thiamine transporter 1
Cyclic nucleotide–gated ion channel