Evidence map›Paper›PMID 25619798›Full record

ReviewCNS spectrums2016

Ameliorating treatment-refractory depression with intranasal ketamine: potential NMDA receptor actions in the pain circuitry representing mental anguish.

Lewis A Opler, Mark G A Opler, Amy F T Arnsten

Abstract readReview
In one paragraph

Review in CNS spectrums, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.4field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  11. Serial Prefrontal Pathways Are Positioned to Balance Cognition and Emotion in Primates.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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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

3 authors at 2 institutions in 1 country.

Lewis A Opler1Department of Psychiatry,Columbia University Medical Center,New York,New York,USA.
Mark G A Opler1Department of Psychiatry,Columbia University Medical Center,New York,New York,USA.
Amy F T Arnsten4Department of Neurobiology,Yale University School of Medicine,New Haven,Connecticut,USA.
Columbia University Irving Medical Center · USYale University · US

Funding

Highly evolved brain circuits in primates: molecular vulnerabilities for diseaseDP1AG047744 · NIA · YALE UNIVERSITY · PI ARNSTEN, AMY F.T. · 2013 to 2017
$4.1M
NIA NIH HHS DP1 AG047744
6 · The paper itself

Abstract

This article reviews the antidepressant actions of ketamine, an N-methyl-D-aspartame glutamate receptor (NMDAR) antagonist, and offers a potential neural mechanism for intranasal ketamine's ultra-rapid actions based on the key role of NMDAR in the nonhuman primate prefrontal cortex (PFC). Although intravenous ketamine infusions can lift mood within hours, the current review describes how intranasal ketamine administration can have ultra-rapid antidepressant effects, beginning within minutes (5-40 minutes) and lasting hours, but with repeated treatments needed for sustained antidepressant actions. Research in rodents suggests that increased synaptogenesis in PFC may contribute to the prolonged benefit of ketamine administration, beginning hours after administration. However, these data cannot explain the relief that occurs within minutes of intranasal ketamine delivery. We hypothesize that the ultra-rapid effects of intranasal administration in humans may be due to ketamine blocking the NMDAR circuits that generate the emotional representations of pain (eg, Brodmann Areas 24 and 25, insular cortex), cortical areas that can be overactive in depression and which sit above the nasal epithelium. In contrast, NMDAR blockade in the dorsolateral PFC following systemic administration of ketamine may contribute to cognitive deficits. This novel view may help to explain how intravenous ketamine can treat the symptoms of depression yet worsen the symptoms of schizophrenia.

Indexed as

Administration, IntranasalAnimalsCerebral CortexDepressive Disorder, Treatment-ResistantExcitatory Amino Acid AntagonistsHumansKetaminePainPrefrontal CortexReceptors, N-Methyl-D-AspartateSynapsesExcitatory Amino Acid AntagonistsKetamineReceptors, N-Methyl-D-AspartateAntidepressantarea 25glutamateprefrontal cortexrTMS

Identifiers

PMID25619798
PMCPMC4515405
OpenAlexW2109249243

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.