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Conversely, when the copper chelator bathocuproine disulfate (BCS) was applied to cultures to reduce intracellular copper prior to exposure glutamate/glycine, neuronal death was increased (Schlief et al., 2006)

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A pharmacologic strategy for overcoming limited NAC BBB permeability and/or active efflux out of the brain includes co-administration with the membrane transporter inhibitor probenecid, a classic and promiscuous ATP-binding cassette (ABC), and solute carrier (SLC) inhibitor that blocks transport of organic acids [6]