The effects of a subanesthetic dose of ketamine on verbal memory in normal volunteers

Parwani, Arti; Weiler, Martin; Blaxton, Teresa A.; Warfel, Dale; Hardin, Michael; Frey, Kristin; Lahti, Adrienne C.

doi:10.1007/s00213-005-0177-2

Cited by 86 publications

(60 citation statements)

References 30 publications

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“…In laboratory experiments, a subanesthetic dose of ketamine given to normal volunteers induces the symptoms of schizophrenia more effectively than any other known drug [29][30][31][32]. NMDA antagonists reproduce both negative and positive symptoms, as well as many of the cognitive deficits associated with the disease.…”

Section: Nmda Hypofunctionmentioning

confidence: 99%

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Lisman

Coyle

Green

et al. 2008

Trends in Neurosciences

913

824

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Many risk genes interact synergistically to produce schizophrenia and many neurotransmitter interactions have been implicated. We have developed a circuit-based framework for understanding gene and neurotransmitter interactions. NMDAR hypofunction has been implicated in schizophrenia because NMDAR antagonists reproduce symptoms of the disease. One action of antagonists is to reduce the excitation of fast-spiking interneurons, resulting in disinhibition of pyramidal cells. Overactive pyramidal cells, notably those in the hippocampus, can drive a hyperdopaminergic state that produces psychosis. Additional aspects of interneuron function can be understood in this framework, as follows. (i) In animal models, NMDAR antagonists reduce parvalbumin and GAD67, as found in schizophrenia. These changes produce further disinhibition and can be viewed as the aberrant response of a homeostatic system having a faulty activity sensor (the NMDAR). (ii) Disinhibition decreases the power of gamma oscillation and might thereby produce negative and cognitive symptoms. (iii) Nicotine enhances the output of interneurons, and might thereby contribute to its therapeutic effect in schizophrenia.

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Section: Nmda Hypofunctionmentioning

confidence: 99%

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Lisman

Coyle

Green

et al. 2008

Trends in Neurosciences

913

824

View full text Add to dashboard Cite

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“…At low doses, ketamine interfered primarily with early consolidation of memory, reducing the delayed recall of words presented immediately before but not during infusion of the drug. 60 Different doses of anesthetics have different effects on the time-dependent types of memory. Generally, low doses of anesthetics leave very short-term memory intact, such that patients can carry on a conversation and appear to be lucid.…”

Section: Blockade Of Memory By General Anesthetics In Humans and Labomentioning

confidence: 99%

Inhibition of learning and memory by general anesthetics

Wang

Orser

2010

Can J Anesth/J Can Anesth

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“…In healthy volunteers, ketamine reliably results in acute impairments in learning and memory (Krystal et al, 1994;Krystal et al, 1999;Krystal et al, 2005;Morgan et al, 2004;Parwani et al, 2005;Perry et al, 2007). Most studies of neurocognition in healthy volunteers have utilized a dosing strategy distinct from what has been utilized in clinical trials for depression to date.…”

Section: Introductionmentioning

confidence: 99%

“…For example, Krystal et al (2005) used a 1-min IV infusion of 0.23 mg/kg of ketamine followed by a 1-h infusion of 0.5 mg/kg in a neurocognitive study in healthy volunteers and assessments were conducted during the drug infusion. Some studies have found evidence for selective impairments in aspects of executive functioning related to ketamine (Krystal et al, 1994;Krystal et al, 1999), whereas other studies have found no impairments (Morgan et al, 2004;Parwani et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Neurocognitive Effects of Ketamine and Association with Antidepressant Response in Individuals with Treatment-Resistant Depression: A Randomized Controlled Trial

Murrough

Burdick

Levitch

et al. 2014

Neuropsychopharmacol

115

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The glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine displays rapid antidepressant effects in patients with treatment-resistant depression (TRD); however, the potential for adverse neurocognitive effects in this population has not received adequate study. The current study was designed to investigate the delayed neurocognitive impact of ketamine in TRD and examine baseline antidepressant response predictors in the context of a randomized controlled trial. In the current study, 62 patients (mean age ¼ 46.2 ± 12.2) with TRD free of concomitant antidepressant medication underwent neurocognitive assessments using components of the MATRICS Consensus Cognitive Battery (MCCB) before and after a single intravenous infusion of ketamine (0.5 mg/kg) or midazolam (0.045 mg/kg). Participants were randomized to ketamine or midazolam in a 2:1 fashion under double-blind conditions and underwent depression symptom assessments at 24, 48, 72 h, and 7 days post treatment using the Montgomery-Asberg Depression Rating Scale (MADRS). Post-treatment neurocognitive assessment was conducted once at 7 days. Neurocognitive performance improved following the treatment regardless of treatment condition. There was no differential effect of treatment on neurocognitive performance and no association with antidepressant response. Slower processing speed at baseline uniquely predicted greater improvement in depression at 24 h following ketamine (t ¼ 2.3, p ¼ 0.027), while controlling for age, depression severity, and performance on other neurocognitive domains. In the current study, we found that ketamine was devoid of adverse neurocognitive effects at 7 days post treatment and that slower baseline processing speed was associated with greater antidepressant response. Future studies are required to further define the neurocognitive profile of ketamine in clinical samples and to identify clinically useful response moderators.

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The effects of a subanesthetic dose of ketamine on verbal memory in normal volunteers

Abstract: This study characterizes the behavioral effects associated with ketamine and suggests that ketamine decreases verbal memory performance by interfering with early consolidation processes.

Cited by 86 publications

References 30 publications

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Inhibition of learning and memory by general anesthetics

Neurocognitive Effects of Ketamine and Association with Antidepressant Response in Individuals with Treatment-Resistant Depression: A Randomized Controlled Trial

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