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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Addict Biol. 2012 Sep 27;19(1):10.1111/j.1369-1600.2012.00506.x. doi: 10.1111/j.1369-1600.2012.00506.x

Figure 3.

Figure 3

Modafinil increases in glutamate were abolished by CPG and conotoxin, and were partly antagonized by TTX. A) CPG (1μM, filled arrow; a cystine-glutamate exchange inhibitor) was introduced into the dialysis buffer 60 min prior to injecting modafinil (open arrow) and prevented the rise in glutamate, indicating dependence of this effect on cysteine-glutamate exchange. B) AIDA (300 μM; a mGluR1 antagonist) was without effect on modafinil-induced glutamate. C) TTX (3 μM; a voltage-dependent sodium channel inhibitor) produced a partial reduction in modafinil-induced glutamate, indicating partial mediation of this effect by impulse-dependent glutamate release. D) Conotoxin [10 μM; a voltage gated calcium channel (Cav) inhibitor] prevented modafinil-mediated increases in glutamate, suggesting dependence of this effect upon Cav. The aCSF group is repeated in each panel. *p <0.05 compared to aCSF group, + p< 0.05 compared to baseline within group.