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Carolyn I. Rodriguez

2 papers in the library · 2 citations · publishing 2020-2021

Papers

Acute Ketamine Modulated Functional Brain Coupling and Dissociative and Affective States in Human Subjects: Interim Analyses

bioRxiv Preprint Server September 20, 2021 Laura M. Hack, Katherine G. Warthen, Xue Zhang et al. 2 citations preprint

Ketamine, a drug used for depression and anesthesia, causes dose-dependent increases in dissociation and intoxication, reduces emotional insensitivity, and raises stress as measured by cortisol. It alters brain connectivity, particularly between reward and negative affect circuits and thalamic sub-regions. Increased coupling between the amygdala and anteroventral thalamus correlates with greater dissociation and intoxication, while decreased coupling of anteromedial and posterior parietal thalamus correlates with increased sensory reward responsiveness. Drug-altered connectivity involving the nucleus accumbens and thalamic sub-regions shows negative associations with anxiety. These findings help disentangle the brain states underlying ketamine's acute effects, informing its therapeutic use and abuse risk.

Ketamine increases activity of a fronto-striatal projection that regulates compulsive behavior

bioRxiv Preprint Server July 6, 2020 Gwynne L. Davis, Adelaide R. Minerva, Argentina Lario et al. preprint

Ketamine rapidly reduces compulsive grooming in a mouse model of obsessive-compulsive disorder by increasing activity in a specific brain circuit connecting the dorsomedial prefrontal cortex to the dorsomedial striatum. Optogenetically mimicking this increased fronto-striatal activity also rescued compulsive behavior, while inhibiting this circuit in normal mice increased grooming. These findings suggest this neural pathway may underlie ketamine's fast-acting therapeutic effects in OCD.