Evidence map›Paper›PMID 38496451›Full record

ArticlebioRxiv : the preprint server for biology2024

Opioid receptor expressing neurons of the central amygdala gate behavioral effects of ketamine in mice.

Matthew B Pomrenze, Sam Vaillancourt, Pierre Llorach, Daniel Ryskamp Rijsketic, Austen B Casey, Nicholas Gregory, Juliana S Salgado, Robert C Malenka, Boris D Heifets

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Matthew B PomrenzeNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305.ORCID 0000-0002-9032-5911
Sam VaillancourtDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Pierre LlorachDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-4457-7800
Daniel Ryskamp RijsketicDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-2197-0730
Austen B CaseyDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-4670-851X
Nicholas GregoryDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0001-9392-6504
Juliana S SalgadoDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Robert C MalenkaNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305.ORCID 0000-0002-5428-5211
Boris D HeifetsDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0003-1474-0379
Stanford University · US

Funding

Training CoreP50DA042012 · NIDA · STANFORD UNIVERSITY · PI Karl A. Deisseroth · 2017 to 2026
$27.1M
Mapping Neural Circuit Activity Mediating MDMA's Prosocial EffectR01MH130591 · NIMH · STANFORD UNIVERSITY · PI Boris Dov Heifets · 2023 to 2026
$2.3M
Neural circuitry and synaptic physiology underlying MDMA's prosocial effectK08MH110610 · NIMH · STANFORD UNIVERSITY · PI HEIFETS, BORIS DOV · 2017 to 2020
$780k
Lightsheet Microscope for Large-Scale Imaging of Cleared Tissue SamplesS10OD025091 · OD · STANFORD UNIVERSITY · PI DEISSEROTH, KARL A. · 2018 to 2018
$337k
Modulation of protracted opioid withdrawal by dorsal raphe dynorphin neuronsK99DA056573 · NIDA · STANFORD UNIVERSITY · PI POMRENZE, MATTHEW B · 2022 to 2023
$317k
NIDA NIH HHS K99 DA056573NIDA NIH HHS P50 DA042012NIH HHS S10 OD025091NIMH NIH HHS K08 MH110610NIMH NIH HHS R01 MH130591
6 · The paper itself

Abstract

Ketamine has anesthetic, analgesic, and antidepressant properties which may involve multiple neuromodulatory systems. In humans, the opioid receptor (OR) antagonist naltrexone blocks the antidepressant effect of ketamine. It is unclear whether naltrexone blocks a direct effect of ketamine at ORs, or whether normal functioning of the OR system is required to realize the full antidepressant effects of treatment. In mice, the effect of ketamine on locomotion, but not analgesia or the forced swim test, was sensitive to naltrexone and was therefore used as a behavioral readout to localize the effect of naltrexone in the brain. We performed whole-brain imaging of cFos expression in ketamine-treated mice, pretreated with naltrexone or vehicle, and identified the central amygdala (CeA) as the area with greatest difference in cFos intensity. CeA neurons expressing both μOR (MOR) and PKCμ were strongly activated by naltrexone but not ketamine, and selectively interrupting MOR function in the CeA either pharmacologically or genetically blocked the locomotor effects of ketamine. These data suggest that MORs expressed in CeA neurons gate behavioral effects of ketamine but are not direct targets of ketamine.

Identifiers

PMID38496451
PMCPMC10942405
OpenAlexW4392520252

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.