Evidence map›Paper›PMID 25754145›Full record

ReviewNeuroscience bulletin2015

Contribution of NMDA receptors to dorsolateral prefrontal cortical networks in primates.

Min Wang, Amy F T Arnsten

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience bulletin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Blockage of NMDA- and GABA(A) Receptors Improves Working Memory Selectivity of Primate Prefrontal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  11. Article
  12. Plasticity of Persistent Activity and Its Constraints.Frontiers in neural circuits · 2020
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Min WangDepartment of Neurobiology, Yale Medical School, New Haven, CT, 06510, USA, Min.wang@yale.edu.
Amy F T Arnsten
Yale University · US

Funding

Nicotinic Receptor Influences on Neuronal Physiology in Dorsolateral Prefrontal CR01MH093354 · NIMH · YALE UNIVERSITY · PI WANG, MIN · 2012 to 2020
$3.8M
NIMH NIH HHS R01 MH093354NIMH NIH HHS R01 MH 09335401
6 · The paper itself

Abstract

Cognitive disorders such as schizophrenia and Alzheimer's disease are associated with dysfunction of the highly evolved dorsolateral prefrontal cortex (dlPFC), and with changes in glutamatergic N-methyl-D-aspartate receptors (NMDARs). Recent research on the primate dlPFC discovered that the pyramidal cell circuits that generate the persistent firing underlying spatial working memory communicate through synapses on spines containing NMDARs with NR2B subunits (GluN2B) in the post-synaptic density. This contrasts with synapses in the hippocampus and primary visual cortex, where GluN2B receptors are both synaptic and extrasynaptic. Blockade of GluN2B in the dlPFC markedly reduces the persistent firing of the Delay cells needed for neuronal representations of visual space. Cholinergic stimulation of nicotinic α7 receptors within the glutamate synapse is necessary for NMDAR actions. In contrast, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors have only subtle effects on the persistent firing of Delay cells, but contribute substantially to the firing of Cue and Response cells. Systemic administration of the NMDAR antagonist ketamine reduces the persistent firing of Delay cells, but increases the firing of some Response cells. The reduction in persistent firing produced by ketamine may explain why this drug can mimic or worsen the cognitive symptoms of schizophrenia. Similar actions in the medial PFC circuits representing the emotional aspects of pain may contribute to the rapid analgesic and anti-depressant actions of ketamine.

Indexed as

Action PotentialsAnimalsHumansMental DisordersNerve NetNeuronal PlasticityNeuronsPrefrontal CortexPrimatesReceptors, N-Methyl-D-AspartateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID25754145
PMCPMC4734117
OpenAlexW2007380470

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.