Rationale: N-methyl-D-aspartate (NMDA) receptor antagonists (e.g., PCP, ketamine) have been shown to impair learning/memory. Well documented in animal models, only limited research in humans has been reported. Findings to date are similar to results of animal studies; however, antagonists are typically administered before the learning experience. This may be problematic as memory failure could be secondary to inattention induced by the psychotomimetic effects of these drugs and/or alterations in sensory processing which can degrade the quality of the stimulus, thereby affecting the accuracy of recall.
Objective: The objective of the study is to compare the effects of ketamine vs placebo on recall for words when administered after stimulus presentation.
Methods: In this double-blind crossover study, 24 normal controls were given bolus injections of ketamine (0.3 mg/kg) or placebo. Immediately prior to infusion, subjects were administered a verbal memory test. Delayed recall was measured 45 min postinfusion. Mental status changes were assessed using the Brief Psychiatric Rating Scale.
Results: Subjects experienced a significant increase in psychiatric symptoms that peaked at 20 min. Results indicate no differences between the drug and placebo conditions for the memory task. However, reminiscence (i.e., recall of previously unrecalled items with repeated testing) was significantly reduced following ketamine administration compared to placebo.
Conclusions: Findings suggest that aspects of memory consolidation are affected by drugs that interfere with NMDA receptor function.
Introduction: Psychedelic-induced experiences are thought to play an important role in the therapeutic actions of rapid-acting antidepressants. General anesthesia is one scenario in which patients can be rendered unconscious and masked to the psychedelic treatment, providing a simple yet effective method to examine drug-induced changes in the brain devoid of experiences.
Methods: Chronically stressed adult C57/BL6 male mice were given subhypnotic ketamine alone or ketamine and GABAergic anesthetic isoflurane at sedative (0.
Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan; Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. Electronic address:
Postoperative cognitive dysfunction (POCD) is characterized by a decline in cognitive functions, including memory, attention, and executive abilities, following surgery, with no effective therapeutic drugs currently available. Arketamine, the (R)-enantiomer of ketamine, has shown promise in mitigating cognitive deficits in animal models. In this study, we investigated whether arketamine could ameliorate cognitive deficits in a mouse model of POCD, with a focus on the role of transforming growth factor (TGF)-β1 in its effects.
This study presents the first in vivo measurement of transcytolemmal water exchange in the brain using a novel Magnetic Resonance technique. We extend previous applications of Chemical Exchange Saturation Transfer (CEST) to examine water exchange across cellular membranes in late-stage chicken embryo brains. The immature blood-brain barrier at this stage allows Gadolinium-Based Contrast Agents (GBCAs) to penetrate the brain's interstitial space, sensitizing the CEST effect to water exchange between intra- and extracellular environments.
Ketamine displays efficacious rapid-acting antidepressant (RAAD) activity in the rat chronic mild stress (CMS) model. It rapidly reverses anhedonia (CMS-induced sucrose consumption deficit) and attenuates working memory deficit (novel object recognition: NOR) following both systemic (intraperitoneal, i.p.
