Evidence map›Paper›PMID 39099429›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Oxytocin Protects Nigrostriatal Dopamine Signal via Activating GABAergic Circuit in the MPTP-Induced Parkinson's Disease Model.

Yurong Wang, Hao Xu, Saiyong Chen, Junhao Chen, Qimeng Zheng, Yuanyuan Ma, Xinru Zhao, Ying Shi, Lei Xiao

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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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

9 authors.

Yurong WangShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Hao XuShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Saiyong ChenShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Junhao ChenShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Qimeng ZhengShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Yuanyuan MaShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Xinru ZhaoShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Ying ShiShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Lei XiaoShanghai Stomatological Hospital & School of Stomatology, The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.ORCID 0000-0002-6897-4608

Funding

Lingang Laboratory LG-QS-202203-12National Natural Science Foundation of China 31900738National Natural Science Foundation of China 32371058National Natural Science Foundation of China 81970727Shanghai Center for Brain Science and Brain-Inspired TechnologyShanghai Municipal Science and Technology Major Project 2018SHZDZX01
6 · The paper itself

Abstract

The most pronounced neuropathological feature of Parkinson's disease (PD) is the loss of dopamine (DA) neurons in the substantia nigra compacta (SNc), which depletes striatal DA. Hypothalamic oxytocin is found to be reduced in PD patients and closely interacts with the DA system, but the role of oxytocin in PD remains unclear. Here, the disturbances of endogenous oxytocin level and the substantia nigra (SN) oxytocin receptor expression in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model is observed, correlated with the striatal tyrosine hydroxylase (TH) expression reduction. Killing/silencing hypothalamic oxytocin neurons aggravates the vulnerability of nigrostriatal DA signal to MPTP, whereas elevating oxytocin level by intranasal delivery or microinjecting into the SN promotes the resistance. In addition, knocking out SN oxytocin receptors induces the time-dependent reductions of SNc DA neurons, striatal TH expression, and striatal DA level by increasing neuronal excitotoxicity. These results further uncover that oxytocin dampens the excitatory synaptic inputs onto DA neurons via activating oxytocin receptor-expressed SN GABA neurons, which target GABA(B) receptors expressed in SNc DA neuron-projecting glutamatergic axons, to reduce excitotoxicity. Thus, besides the well-known prosocial effect, oxytocin acts as a key endogenous factor in protecting the nigrostriatal DA system.

Indexed as

Corpus StriatumDisease Models, AnimalDopamineMice, Inbred C57BLOxytocinSubstantia Nigra1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsDopaminergic NeuronsGABAergic NeuronsMaleMiceParkinson DiseaseReceptors, Oxytocin1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineDopamineOxytocinReceptors, OxytocinDopamineExcitatory synaptic transmissionGABA(B) receptorintranasal deliveryOxytocinParkinson's disease

Identifiers

PMID39099429
PMCPMC11423065

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.