Living organisms rely on selective attention to navigate through abundant sensory information efficiently. While the cortical networks of selective attention have been extensively studied, the role of the major inhibitory neurotransmitter γ-aminobutyric acid (GABA) is less well understood. Increased GABA_A receptor activity due to benzodiazepine administration such as lorazepam has long been known to slow down psychomotor performance and in a previous study, we have obtained first evidence that increased GABA_A receptor activity may impair selective attention. However, it remained unclear, whether observed impairments stem from a slowed build-up of selectivity, consistent with benzodiazepine induced slowing of other processes, or from a generally widened attentional focus. To address this gap, N=29 healthy participants received lorazepam (1mg; placebo-controlled, within-subjects design) and performed an extended version of the arrowed flanker task, systematically varying the number an position of incongruent flankers. Under lorazepam, incongruent flankers close to the target impaired performance more strongly than flankers located more distantly, whereas under placebo only the number of incongruent flankers, but not their position, had an significant effect. Delta plot analyses of reaction time showed that this effect persisted for slow reactions, suggesting a widening of attentional focus that is distinct from general mechanisms of slowing. These findings underscore the role of GABAergic modulation in selective attentional processes and highlight the need for further exploration into neurotransmitter systems underlying selective attention.