Evidence map›Paper›PMID 35649726›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022

NMDA Receptors in the Lateral Preoptic Hypothalamus Are Essential for Sustaining NREM and REM Sleep.

Giulia Miracca, Berta Anuncibay-Soto, Kyoko Tossell, Raquel Yustos, Alexei L Vyssotski, Nicholas P Franks, William Wisden

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  4. Gene-by-Sleep Duration Interaction for Glycemic Traits in over 480,000 Individuals.medRxiv : the preprint server for health sciences · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Giulia MiraccaDepartment of Life Sciences, Imperial College London, London SW7 2AZ, United Kingdom.
Berta Anuncibay-SotoDepartment of Life Sciences, Imperial College London, London SW7 2AZ, United Kingdom.
Kyoko TossellDepartment of Life Sciences, Imperial College London, London SW7 2AZ, United Kingdom.
Raquel YustosDepartment of Life Sciences, Imperial College London, London SW7 2AZ, United Kingdom.ORCID https://orcid.org/0000-0001-9387-242X
Alexei L VyssotskiInstitute of Neuroinformatics, University of Zürich/Eidgenössische Technische Hochschule Zürich, Zürich CH-8057, Switzerland.
Nicholas P FranksDepartment of Life Sciences, Imperial College London, London SW7 2AZ, United Kingdom n.franks@imperial.ac.uk w.wisden@imperial.ac.uk.ORCID https://orcid.org/0000-0003-4874-4212
William WisdenDepartment of Life Sciences, Imperial College London, London SW7 2AZ, United Kingdom n.franks@imperial.ac.uk w.wisden@imperial.ac.uk.ORCID https://orcid.org/0000-0003-4743-0334
Imperial College London · GBUK Dementia Research Institute · GBUniversity of Zurich · CH

Funding

Wellcome Trust 107839/Z/15/ZWellcome Trust 107841Wellcome Trust 107841/Z/15/ZWellcome Trust 220759
6 · The paper itself

Abstract

The lateral preoptic (LPO) hypothalamus is a center for NREM and REM sleep induction and NREM sleep homeostasis. Although LPO is needed for NREM sleep, we found that calcium signals were, surprisingly, highest in REM sleep. Furthermore, and equally surprising, NMDA receptors in LPO were the main drivers of excitation. Deleting the NMDA receptor GluN1 subunit from LPO abolished calcium signals in all cells and produced insomnia. Mice of both sexes had highly fragmented NREM sleep-wake patterns and could not generate conventionally classified REM sleep. The sleep phenotype produced by deleting NMDA receptors depended on where in the hypothalamus the receptors were deleted. Deleting receptors from the anterior hypothalamic area (AHA) did not influence sleep-wake states. The sleep fragmentation originated from NMDA receptors on GABA neurons in LPO. Sleep fragmentation could be transiently overcome with sleeping medication (zolpidem) or sedatives (dexmedetomidine; Dex). By contrast, fragmentation persisted under high sleep pressure produced by sleep deprivation (SD), mice had a high propensity to sleep but woke up. By analyzing changes in δ power, sleep homeostasis (also referred to as "sleep drive") remained intact after NMDA receptor ablation. We suggest NMDA glutamate receptor activation stabilizes firing of sleep-on neurons and that mechanisms of sleep maintenance differ from that of the sleep drive itself.

Indexed as

Sleep Initiation and Maintenance DisordersSleep, REMAnimalsCalciumElectroencephalographyFemaleHypothalamusMaleMiceN-MethylaspartateReceptors, N-Methyl-D-AspartateSleepSleep DeprivationWakefulnessCalciumN-MethylaspartateReceptors, N-Methyl-D-AspartatehypothalamusNMDA receptorNREMpreopticREMsleep

Identifiers

PMID35649726
PMCPMC7613025
OpenAlexW4281941124

What OpenQuestion holds

Textmetadata
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.