Evidence map›Paper›PMID 30131699›Full record

ArticleFrontiers in pharmacology2018

EphB2 Deficiency Induces Depression-Like Behaviors and Memory Impairment: Involvement of NMDA 2B Receptor Dependent Signaling.

Linlin Zhen, Tuo Shao, Victor Luria, Gaowen Li, Zhi Li, Ying Xu, Xin Zhao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  4. The Eph-ephrin system in neuropsychiatric and neurodevelopmental disorders.Journal of psychiatry & neuroscience : JPN · 2026
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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

7 authors at 7 institutions in 2 countries.

Linlin ZhenDepartment of Breast and Thyroid Surgery, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, China.
Tuo ShaoBrain Institute, School of Pharmacy, Wenzhou Medical University, Wenzhou, China.
Victor LuriaDepartment of Systems Biology, Harvard University Medical School, Boston, MA, United States.
Gaowen LiDepartment of Pharmacology, Ningbo College of Health Sciences, Ningbo, China.
Zhi LiDepartment of Breast and Thyroid Surgery, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, China.
Ying XuSchool of Pharmacy and Pharmaceutical Sciences, University at Buffalo, State University of New York, Buffalo, NY, United States.
Xin ZhaoDepartment of Pharmacology, School of Medical Science, Ningbo University, Ningbo, China.
Harvard University · USNingbo College of Health Sciences · CNNingbo University · CNSecond People’s Hospital of Huai’an · CNUniversity at Buffalo, State University of New York · USWenzhou Medical University · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Receptor tyrosine kinase EphB2 mediates development of the neurogenic niche of excitatory neurons, suggesting the possibility that its inactivation plays a role in neuropsychiatric disorders including depression and memory impairment. While N-methyl-D-aspartate (NMDA) receptor is involved in regulating memory formation and neurogenesis in adult animal, it remains unclear how NMDA receptor subtypes mediate depression and cognitive deficits caused by EphB2 loss. The present study shows that EphB2 inactivation results in depression-like behaviors, memory impairment and defects of adult hippocampal neurogenesis. Compared to wild-type littermates, EphB2 KO mice exhibited depression-like behavior and deficits in spatial memory and cognition in forced swimming, tail suspension, Morris water maze, object recognition test and object location test. These behavioral abnormalities were accompanied by substantial decreases in the number of BrdU+ progenitor neurons, phosphorylation of cAMP-response element binding protein (pCREB) and brain derived neurotrophic factor (BDNF), and increased NMDA receptor 2B (NR2B) expression. These molecular, cellular and behavioral alterations induced by EphB2 inactivation were reversed by NR2B antagonist Ro25-6981, suggesting that EphB2 functions to prevent the progression of depression-like behavior and memory impairment by downregulating NR2B. Our findings highlight that NR2B is responsible for EphB2-dependent behavioral and morphological changes. EphB2 may thus be as an important candidate target for treating psychiatric and cognitive disorders.

Indexed as

cognitiondepressionEphB2neurogenesisNMDA-2B receptorNR2B antagonist Ro25-6981

Identifiers

PMID30131699
PMCPMC6090375
OpenAlexW2887888384

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.