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This study is the first randomized controlled trial to test the effects of ketamine in Borderline Personality Disorder (BPD). BPD remains undertreated in the community and no medication has FDA approval for this indication. People with BPD experience chronic mood disturbances with depressed mood, suicidal ideation, and severe social difficulties. In this double-blind, randomized controlled pilot study, we tested the effects of one infusion of ketamine (0.5 mg/kg, n = 10) or the psychoactive comparator drug midazolam (0.04 mg/kg, n = 12) in adults with BPD. Infusions were well tolerated in both groups. Dissociative symptoms during infusion were more intense with ketamine than midazolam (t(12.3) = 3.61, p = 0.01), but they resolved by 40 min after infusion in both groups. Post-infusion adverse events were at the expected low levels in both groups. For our primary outcome measure of suicidal ideation and our secondary outcome measure of depression, we found numerical reduction but not significant group or group x timepoint difference (p > 0.05). For our secondary outcome measures of anxiety and BPD symptoms, we did not observe group or group x timepoint differences. There was a group x timepoint effect for socio-occupational functioning (F(1,20.12) = 5.16, p = 0.03, at Day 14, ketamine group showed more improvement than midazolam group). An exploratory analysis revealed that improvement in socio-occupational functioning was correlated with improvement in depression in the ketamine group (r(8) = 0.65, p = 0.04) but not midazolam group (r(9) = 0.41, p = 0.216). This pilot study provides the first randomized controlled evidence of the effects of antidepressant-dosed ketamine in people with BPD. Our results provide reason for optimism that antidepressant-dosed ketamine will be well-tolerated in larger studies and may provide clinical benefit for mood symptoms and related impairments in people with BPD.

The amygdala and hippocampus are central to emotional processing, yet the transient neural dynamics coordinating these regions remain unclear. We simultaneously recorded single-neuron activity and local field potentials from both regions in epilepsy patients during an emotional image-rating task. Neurons in both regions responded to images with firing rate changes that predicted subjective ratings of extreme pleasantness or unpleasantness. To examine the underlying oscillatory mechanisms, we analyzed beta bursts (13-30 Hz)-transient, high-power events-since conventional spectral analyses revealed no valence-specific patterns. Beta bursts were associated with increased gamma amplitude and enhanced phase coherence in both structures, with beta-gamma phase-amplitude coupling capturing emotion-related dynamics. Critically, amygdala beta bursts strongly suppressed hippocampal firing through interneuron activation during negative valence processing, whereas hippocampal bursts showed no reciprocal influence. These findings suggest that beta bursts provide a temporal code for emotion and represent a candidate mechanism for targeted neuromodulation in mood disorders.