Evidence map›Paper›PMID 37301901›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2023

The effect of ketamine on synaptic mistuning induced by impaired glutamate reuptake.

Erika Vazquez-Juarez, Ipsit Srivastava, Maria Lindskog

Abstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Ketamine and Evolving Neuroplasticity.Clinical drug investigation · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. 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

3 authors.

Erika Vazquez-JuarezDepartment of Neurobiology, Care Sciences and Society, Karolinska Institutet, 171 77, Stockholm, Sweden.
Ipsit SrivastavaDepartment of Neurobiology, Care Sciences and Society, Karolinska Institutet, 171 77, Stockholm, Sweden.
Maria LindskogDepartment of Neurobiology, Care Sciences and Society, Karolinska Institutet, 171 77, Stockholm, Sweden. mia.lindskog@uu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mistuning of synaptic transmission has been proposed to underlie many psychiatric disorders, with decreased reuptake of the excitatory neurotransmitter glutamate as one contributing factor. Synaptic tuning occurs through several diverging and converging forms of plasticity. By recording evoked field postsynaptic potentials in the CA1 area in hippocampal slices, we found that inhibiting glutamate transporters using DL-TBOA causes retuning of synaptic transmission, resulting in a new steady state with reduced synaptic strength and a lower threshold for inducing long-term synaptic potentiation (LTP). Moreover, a similar reduced threshold for LTP was observed in a rat model of depression with decreased levels of glutamate transporters. Most importantly, we found that the antidepressant ketamine counteracts the effects of increased glutamate on the various steps involved in synaptic retuning. We, therefore, propose that ketamine's mechanism of action as an antidepressant is to restore adequate synaptic tuning.

Indexed as

KetamineAnimalsAntidepressive AgentsGlutamatesHippocampusHumansLong-Term PotentiationRatsSynapsesSynaptic TransmissionAntidepressive AgentsGlutamatesKetamine

Identifiers

PMID37301901
PMCPMC10584870

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.