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NMDA Receptors Subserve Persistent Neuronal Firing during Working Memory in Dorsolateral Prefrontal Cortex

Neurons in the primate dorsolateral prefrontal cortex (dlPFC) generate persistent firing in the absence of sensory stimulation, the foundation of mental representation. Persistent firing arises from recurrent excitation within a network of pyramidal Delay cells. Here, we examined glutamate receptor... Full description

Journal Title: Neuron 2013, Vol.77 (4), p.736-749
Main Author: Wang, Min
Other Authors: Yang, Yang , Wang, Ching-Jung , Gamo, Nao J , Jin, Lu E , Mazer, James A , Morrison, John H , Wang, Xiao-Jing , Arnsten, Amy F.T
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Elsevier Inc
ID: ISSN: 0896-6273
Link: https://www.ncbi.nlm.nih.gov/pubmed/23439125
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3584418
title: NMDA Receptors Subserve Persistent Neuronal Firing during Working Memory in Dorsolateral Prefrontal Cortex
format: Article
creator:
  • Wang, Min
  • Yang, Yang
  • Wang, Ching-Jung
  • Gamo, Nao J
  • Jin, Lu E
  • Mazer, James A
  • Morrison, John H
  • Wang, Xiao-Jing
  • Arnsten, Amy F.T
subjects:
  • Alzheimer's disease
  • Alzheimers disease
  • Amyloid beta-protein
  • Analysis
  • Animal models
  • Animals
  • Article
  • Brain Mapping
  • Cognition & reasoning
  • Computer Simulation
  • Glutamate
  • Macaca mulatta
  • Male
  • Memory
  • Memory, Short-Term - physiology
  • mental disorders
  • Methyl aspartate
  • Microscopy
  • Models, Neurological
  • Monkeys & apes
  • musculoskeletal
  • nervous system
  • neural
  • Neurons
  • Neurons - physiology
  • Neuroscience(all)
  • Neurosciences
  • ocular physiology
  • Prefrontal Cortex - physiology
  • Primates
  • processes
  • psychological phenomena
  • Pyramidal Cells - physiology
  • Receptors, AMPA - physiology
  • Receptors, N-Methyl-D-Aspartate - physiology
  • Rodents
  • Schizophrenia
  • Short-term memory
  • Studies
ispartof: Neuron, 2013, Vol.77 (4), p.736-749
description: Neurons in the primate dorsolateral prefrontal cortex (dlPFC) generate persistent firing in the absence of sensory stimulation, the foundation of mental representation. Persistent firing arises from recurrent excitation within a network of pyramidal Delay cells. Here, we examined glutamate receptor influences underlying persistent firing in primate dlPFC during a spatial working memory task. Computational models predicted dependence on NMDA receptor (NMDAR) NR2B stimulation, and Delay cell persistent firing was abolished by local NR2B NMDAR blockade or by systemic ketamine administration. AMPA receptors (AMPARs) contributed background depolarization to sustain network firing. In contrast, many Response cells were sensitive to AMPAR blockade and increased firing after systemic ketamine, indicating that models of ketamine actions should be refined to reflect neuronal heterogeneity. The reliance of Delay cells on NMDAR may explain why insults to NMDARs in schizophrenia or Alzheimer’s disease profoundly impair cognition. ► Primate prefrontal cortical working memory circuits require NMDA NR2B receptors ► Blocking NMDA, but not AMPA receptors, markedly reduced Delay cell firing ► Systemic ketamine also reduced Delay cell firing but increased Response cell firing ► These primate data should redefine NMDA glutamate theories of cognitive disorders Wang et al. assess the effect of blocking glutamate receptors on working memory and neuronal firing in primate dlPFC. Delay cell firing is abolished by NMDAR block, while many Response cells are sensitive to AMPAR block. Blocking NR2B receptors impairs working memory, underscoring their role in cognitive function.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0896-6273
fulltext: fulltext
issn:
  • 0896-6273
  • 1097-4199
url: Link


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descriptionNeurons in the primate dorsolateral prefrontal cortex (dlPFC) generate persistent firing in the absence of sensory stimulation, the foundation of mental representation. Persistent firing arises from recurrent excitation within a network of pyramidal Delay cells. Here, we examined glutamate receptor influences underlying persistent firing in primate dlPFC during a spatial working memory task. Computational models predicted dependence on NMDA receptor (NMDAR) NR2B stimulation, and Delay cell persistent firing was abolished by local NR2B NMDAR blockade or by systemic ketamine administration. AMPA receptors (AMPARs) contributed background depolarization to sustain network firing. In contrast, many Response cells were sensitive to AMPAR blockade and increased firing after systemic ketamine, indicating that models of ketamine actions should be refined to reflect neuronal heterogeneity. The reliance of Delay cells on NMDAR may explain why insults to NMDARs in schizophrenia or Alzheimer’s disease profoundly impair cognition. ► Primate prefrontal cortical working memory circuits require NMDA NR2B receptors ► Blocking NMDA, but not AMPA receptors, markedly reduced Delay cell firing ► Systemic ketamine also reduced Delay cell firing but increased Response cell firing ► These primate data should redefine NMDA glutamate theories of cognitive disorders Wang et al. assess the effect of blocking glutamate receptors on working memory and neuronal firing in primate dlPFC. Delay cell firing is abolished by NMDAR block, while many Response cells are sensitive to AMPAR block. Blocking NR2B receptors impairs working memory, underscoring their role in cognitive function.
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subjectAlzheimer's disease ; Alzheimers disease ; Amyloid beta-protein ; Analysis ; Animal models ; Animals ; Article ; Brain Mapping ; Cognition & reasoning ; Computer Simulation ; Glutamate ; Macaca mulatta ; Male ; Memory ; Memory, Short-Term - physiology ; mental disorders ; Methyl aspartate ; Microscopy ; Models, Neurological ; Monkeys & apes ; musculoskeletal ; nervous system ; neural ; Neurons ; Neurons - physiology ; Neuroscience(all) ; Neurosciences ; ocular physiology ; Prefrontal Cortex - physiology ; Primates ; processes ; psychological phenomena ; Pyramidal Cells - physiology ; Receptors, AMPA - physiology ; Receptors, N-Methyl-D-Aspartate - physiology ; Rodents ; Schizophrenia ; Short-term memory ; Studies
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descriptionNeurons in the primate dorsolateral prefrontal cortex (dlPFC) generate persistent firing in the absence of sensory stimulation, the foundation of mental representation. Persistent firing arises from recurrent excitation within a network of pyramidal Delay cells. Here, we examined glutamate receptor influences underlying persistent firing in primate dlPFC during a spatial working memory task. Computational models predicted dependence on NMDA receptor (NMDAR) NR2B stimulation, and Delay cell persistent firing was abolished by local NR2B NMDAR blockade or by systemic ketamine administration. AMPA receptors (AMPARs) contributed background depolarization to sustain network firing. In contrast, many Response cells were sensitive to AMPAR blockade and increased firing after systemic ketamine, indicating that models of ketamine actions should be refined to reflect neuronal heterogeneity. The reliance of Delay cells on NMDAR may explain why insults to NMDARs in schizophrenia or Alzheimer’s disease profoundly impair cognition. ► Primate prefrontal cortical working memory circuits require NMDA NR2B receptors ► Blocking NMDA, but not AMPA receptors, markedly reduced Delay cell firing ► Systemic ketamine also reduced Delay cell firing but increased Response cell firing ► These primate data should redefine NMDA glutamate theories of cognitive disorders Wang et al. assess the effect of blocking glutamate receptors on working memory and neuronal firing in primate dlPFC. Delay cell firing is abolished by NMDAR block, while many Response cells are sensitive to AMPAR block. Blocking NR2B receptors impairs working memory, underscoring their role in cognitive function.
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abstractNeurons in the primate dorsolateral prefrontal cortex (dlPFC) generate persistent firing in the absence of sensory stimulation, the foundation of mental representation. Persistent firing arises from recurrent excitation within a network of pyramidal Delay cells. Here, we examined glutamate receptor influences underlying persistent firing in primate dlPFC during a spatial working memory task. Computational models predicted dependence on NMDA receptor (NMDAR) NR2B stimulation, and Delay cell persistent firing was abolished by local NR2B NMDAR blockade or by systemic ketamine administration. AMPA receptors (AMPARs) contributed background depolarization to sustain network firing. In contrast, many Response cells were sensitive to AMPAR blockade and increased firing after systemic ketamine, indicating that models of ketamine actions should be refined to reflect neuronal heterogeneity. The reliance of Delay cells on NMDAR may explain why insults to NMDARs in schizophrenia or Alzheimer’s disease profoundly impair cognition. ► Primate prefrontal cortical working memory circuits require NMDA NR2B receptors ► Blocking NMDA, but not AMPA receptors, markedly reduced Delay cell firing ► Systemic ketamine also reduced Delay cell firing but increased Response cell firing ► These primate data should redefine NMDA glutamate theories of cognitive disorders Wang et al. assess the effect of blocking glutamate receptors on working memory and neuronal firing in primate dlPFC. Delay cell firing is abolished by NMDAR block, while many Response cells are sensitive to AMPAR block. Blocking NR2B receptors impairs working memory, underscoring their role in cognitive function.
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doi10.1016/j.neuron.2012.12.032
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