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Both pre‐clinical and clinical studies indicate that N‐acetylcysteine (NAC) may be useful in treating relapse to addictive drug use. Cocaine self‐administration in rats reduces both cystine‐glutamate exchange and glutamate transport via GLT‐1 in the nucleus accumbens, and NAC treatment normalizes these two glial processes critical for maintaining glutamate homeostasis. However, it is not known if one or both of these actions by NAC is needed to inhibit relapse to cocaine seeking. To determine whether the restoration of GLT‐1 and/or cystine‐glutamate exchange is required for NAC to inhibit cue‐induced reinstatement of cocaine seeking, we utilized the rat self‐administration/extinction/reinstatement model of cocaine relapse. Rats were pre‐treated in the nucleus accumbens with vivo‐morpholino antisense oligomers targeting either GLT‐1 or xCT (catalytic subunit of the cystine‐glutamate exchanger …