Intro: During binocular rivalry, two dichoptically-presented images are suppressed from perceptual awareness in alternation. Computational models of rivalry (Laing and Chow, 2002; Seely et al., 2011; Said and Heeger, 2013) and magnetic resonance spectroscopy research (Robertson et al., 2016) suggest that the depth of perceptual suppression is governed, in part, by the strength of interocular inhibition in visual cortex. Here, we tested a causal link between the strength of perceptual suppression during rivalry and the inhibitory neurotransmitter, GABA, using pharmacological manipulations. 22 adults participated in each of three separate studies, investigating the effects of a GABA A modulator (Clobazam; study 1), a GABA B modulator (Arbaclofen; study 2), and a Cl-channel modulator (Bumex; study 3) on binocular rivalry dynamics. Each study took place over 3 days: practice session/health assessment (day 1) and two experimental days (day 2-3). On each of the experimental days, a participant was given either a drug or a placebo, and participated in a short binocular rivalry experiment after the drug had taken effect. We found that the GABA A modulator, clobazam, increases perceptual suppression compared with placebo (p< 0.05). Conversely, the Cl-channel modulator, bumetanide, reduces perceptual suppression compared with placebo (p< 0.05). A repeated-measures ANOVA across studies revealed a significant interaction between these two drugs (p< 0.001). Importantly, binocular rivalry dynamics were highly test-retest reliable across testing days (all Rho> 0.65, all p< 0.001). Drowsiness ratings did not influence these results. These findings provide a causal, mechanistic link between the GABA pathway and perceptual suppression, as suggested by our previous Magnetic Resonance Spectroscopy research and computational models of rivalry. Further, these results identify specific aspects of the GABAergic pathway which are involved in supporting binocular rivalry. All in all, our results flag perceptual suppression as a marker of GABAergic drug response.