Prevention of ketamine-induced working memory impairments by AMPA potentiators in a nonhuman primate model of cognitive dysfunction
Working memory impairments are a core aspect of schizophrenia, yet current medicines do not address such cognitive dysfunction. We have developed a model of these working memory deficits by acutely disrupting glutamatergic synaptic transmission by administration of the N-methyl- d-aspartate (NMDA) a...
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Published in | Behavioural brain research Vol. 212; no. 1; pp. 41 - 48 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier B.V
01.09.2010
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Abstract | Working memory impairments are a core aspect of schizophrenia, yet current medicines do not address such cognitive dysfunction. We have developed a model of these working memory deficits by acutely disrupting glutamatergic synaptic transmission by administration of the
N-methyl-
d-aspartate (NMDA) antagonist ketamine in the nonhuman primate. The current studies evaluated the effect of positive allosteric modulators (“potentiators”) of the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors on the working memory and behavioral effects of ketamine. AMPA receptors mediate fast excitatory synaptic transmission throughout the brain and play a critical role in the activity-dependent regulation of NMDA receptors. We find that positive modulation of AMPA receptors with LY451646 (0.1–1.0
mg/kg, SC) and structurally distinct PF-4778574 (0.01
mg/kg, SC) robustly ameliorates ketamine-induced working memory impairments without altering behavioral effects of acute ketamine we consider related to positive- and negative-like symptoms. These results support AMPA receptor potentiators as a potential adjunctive treatment for cognitive impairment associated with schizophrenia (CIAS). |
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AbstractList | Working memory impairments are a core aspect of schizophrenia, yet current medicines do not address such cognitive dysfunction. We have developed a model of these working memory deficits by acutely disrupting glutamatergic synaptic transmission by administration of the
N-methyl-
d-aspartate (NMDA) antagonist ketamine in the nonhuman primate. The current studies evaluated the effect of positive allosteric modulators (“potentiators”) of the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors on the working memory and behavioral effects of ketamine. AMPA receptors mediate fast excitatory synaptic transmission throughout the brain and play a critical role in the activity-dependent regulation of NMDA receptors. We find that positive modulation of AMPA receptors with LY451646 (0.1–1.0
mg/kg, SC) and structurally distinct PF-4778574 (0.01
mg/kg, SC) robustly ameliorates ketamine-induced working memory impairments without altering behavioral effects of acute ketamine we consider related to positive- and negative-like symptoms. These results support AMPA receptor potentiators as a potential adjunctive treatment for cognitive impairment associated with schizophrenia (CIAS). Working memory impairments are a core aspect of schizophrenia, yet current medicines do not address such cognitive dysfunction. We have developed a model of these working memory deficits by acutely disrupting glutamatergic synaptic transmission by administration of the N-methyl-d-aspartate (NMDA) antagonist ketamine in the nonhuman primate. The current studies evaluated the effect of positive allosteric modulators ("potentiators") of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors on the working memory and behavioral effects of ketamine. AMPA receptors mediate fast excitatory synaptic transmission throughout the brain and play a critical role in the activity-dependent regulation of NMDA receptors. We find that positive modulation of AMPA receptors with LY451646 (0.1-1.0mg/kg, SC) and structurally distinct PF-4778574 (0.01mg/kg, SC) robustly ameliorates ketamine-induced working memory impairments without altering behavioral effects of acute ketamine we consider related to positive- and negative-like symptoms. These results support AMPA receptor potentiators as a potential adjunctive treatment for cognitive impairment associated with schizophrenia (CIAS). Working memory impairments are a core aspect of schizophrenia, yet current medicines do not address such cognitive dysfunction. We have developed a model of these working memory deficits by acutely disrupting glutamatergic synaptic transmission by administration of the N-methyl-d-aspartate (NMDA) antagonist ketamine in the nonhuman primate. The current studies evaluated the effect of positive allosteric modulators ("potentiators") of the a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors on the working memory and behavioral effects of ketamine. AMPA receptors mediate fast excitatory synaptic transmission throughout the brain and play a critical role in the activity-dependent regulation of NMDA receptors. We find that positive modulation of AMPA receptors with LY451646 (0.1-1.0mg/kg, SC) and structurally distinct PF-4778574 (0.01mg/kg, SC) robustly ameliorates ketamine-induced working memory impairments without altering behavioral effects of acute ketamine we consider related to positive- and negative-like symptoms. These results support AMPA receptor potentiators as a potential adjunctive treatment for cognitive impairment associated with schizophrenia (CIAS). |
Author | Schmidt, Christopher J. Castner, Stacy A. Seymour, Patricia A. Roberts, Brooke M. Holden, Daniel E. Williams, Graham V. Shaffer, Christopher L. Menniti, Frank S. |
Author_xml | – sequence: 1 givenname: Brooke M. surname: Roberts fullname: Roberts, Brooke M. organization: Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, United States – sequence: 2 givenname: Daniel E. surname: Holden fullname: Holden, Daniel E. organization: Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, United States – sequence: 3 givenname: Christopher L. surname: Shaffer fullname: Shaffer, Christopher L. organization: Neuroscience Research Unit, Pfizer Global Research and Development, Pfizer Inc., Groton, CT 06340, United States – sequence: 4 givenname: Patricia A. surname: Seymour fullname: Seymour, Patricia A. organization: Neuroscience Research Unit, Pfizer Global Research and Development, Pfizer Inc., Groton, CT 06340, United States – sequence: 5 givenname: Frank S. surname: Menniti fullname: Menniti, Frank S. organization: Neuroscience Research Unit, Pfizer Global Research and Development, Pfizer Inc., Groton, CT 06340, United States – sequence: 6 givenname: Christopher J. surname: Schmidt fullname: Schmidt, Christopher J. organization: Neuroscience Research Unit, Pfizer Global Research and Development, Pfizer Inc., Groton, CT 06340, United States – sequence: 7 givenname: Graham V. surname: Williams fullname: Williams, Graham V. organization: Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, United States – sequence: 8 givenname: Stacy A. surname: Castner fullname: Castner, Stacy A. email: stacy.castner@yale.edu organization: Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, United States |
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Keywords | Spatial working memory NMDA Schizophrenia AMPA Ketamine Monkey Memory disorder Cognitive disorder Glutamate receptor Psychosis Prevention Cognitive theory Vertebrata Mammalia Theoretical model General anesthetic Animal Primates Antagonist Working memory NMDA receptor Public health Spatial memory |
Language | English |
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Title | Prevention of ketamine-induced working memory impairments by AMPA potentiators in a nonhuman primate model of cognitive dysfunction |
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