Emerging evidence indicates that many aspects of alcohol and drug dependence 
involve changes in glutamate transmission. A number of studies have reported 
that drugs of abuse, including alcohol and cocaine, alter glutamate transport. 
Extracellular glutamate is regulated by a number of glutamate transporters in 
various brain regions. Of these transporters, glutamate transporter (GLT1) is a 
key player in the removal of most of the extracellular glutamate. Similar to 
neurodegenerative disease models, in which there is dysfunction of the 
glutamatergic excitatory system, the role of GLT1 has been tested in drug 
dependence models that show dysfunction of glutamate transmission. We and others 
have recently found that ceftriaxone, an FDA-approved drug known to elevate GLT1 
expression, attenuates cue-induced cocaine relapse. Moreover, we recently found 
that alcohol-preferring rats treated with ceftriaxone showed a significant 
dosedependent reduction in alcohol consumption. We also demonstrated that 
ceftriaxone-induced upregulation of GLT1 expression was associated with 
increases in glutamate uptake in Huntington's disease mouse model. Importantly, 
ceftriaxone is currently in clinical trials for the treatment of amyotrophic 
lateral sclerosis. This review provides information about the potential 
therapeutic role of GLT1 for the treatment of alcohol abuse and dependence.