Ketamine is a non-competitive NMDA antagonist with hallucinogenic, analgesic and anesthetic properties. It has been repurposed for the treatment of depression, but its narcotic properties have made it attractive for recreational abuse. Consistent with the findings that non-competitive NMDA antagonists disrupt memory, studies in humans and monkeys have demonstrated impartment in cognitive functions, including memory, even with low doses of ketamine. Previously, our laboratory has shown, in macaques, that transient inactivation of the hippocampus by intracerebral infusion of the GABAA agonist muscimol impaired performance in the Hamilton Search Task (HST; a test of non-navigational spatial memory), whereas blockade of cholinergic transmission had no effect. Here we aimed to determine whether a systemic low-dose ketamine affects performance on the same task. Four male macaques (Macaca mulatta, ages 6-13 years) were pretrained on the HST. Subsequently, they received systemic injections of ketamine (0.1, 0.25, 0.5, 1, 2mg/kg) or saline, in a randomized order, 5min before the test on the HST. We found a dose-dependent impairment in several measures: trials to complete starting at 0.25mg/kg (p<0.0001), number of correct responses in the first eight openings at 2mg/kg (p<0.05), and repetition index at 0.5 and 1mg/kg (p<0.001). Higher doses (1 and 2 mg/kg) resulted in motor impairment manifested by an increased latency to reach (p<0.0001). Our results demonstrate that lower doses of ketamine at 0.25 and 0.5mg/kg are sufficient to impair performance on the HST without causing motor impairment. This finding has a translation relevance for dosing of ketamine for treatment in patients.