Evidence map›Paper›PMID 25206424›Full record

ArticleNeural regeneration research2013

Differentiation renders susceptibility to excitotoxicity in HT22 neurons.

Minchao He, Jun Liu, Shaowu Cheng, Yigang Xing, William Z Suo

Open access · greenAbstract read
In one paragraph

Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

33 citing papers in PubMed, 43 citations in OpenAlex.

  1. CRISPR/Cas9-based nanodelivery systems for precision gene editing in neuroinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

5 authors at 1 institution in 1 country.

Minchao HeDepartment of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, Guangdong Province, China ; Laboratory for Alzheimer's Disease & Aging Research, Veterans Affairs Medical Center, Kansas, MO 64128, USA.
Jun LiuDepartment of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, Guangdong Province, China ; Laboratory for Alzheimer's Disease & Aging Research, Veterans Affairs Medical Center, Kansas, MO 64128, USA.
Shaowu ChengLaboratory for Alzheimer's Disease & Aging Research, Veterans Affairs Medical Center, Kansas, MO 64128, USA.
Yigang XingDepartment of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, Guangdong Province, China.
William Z SuoLaboratory for Alzheimer's Disease & Aging Research, Veterans Affairs Medical Center, Kansas, MO 64128, USA ; Department of Neurology, University of Kansas Medical Center, Kansas, KS 66170, USA ; Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas, KS 66170, USA.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HT22 is an immortalized mouse hippocampal neuronal cell line that does not express cholinergic and glutamate receptors like mature hippocampal neurons in vivo. This in part prevents its use as a model for mature hippocampal neurons in memory-related studies. We now report that HT22 cells were appropriately induced to differentiate and possess properties similar to those of mature hippocampal neurons in vivo, such as becoming more glutamate-receptive and excitatory. Results showed that sensitivity of HT22 cells to glutamate-induced toxicity changed dramatically when comparing undifferentiated with differentiated cells, with the half-effective concentration for differentiated cells reducing approximately two orders of magnitude. Moreover, glutamate-induced toxicity in differentiated cells, but not undifferentiated cells, was inhibited by the N-methyl-D- aspartate receptor antagonists MK-801 and memantine. Evidently, differentiated HT22 cells expressed N-methyl-D-aspartate receptors, while undifferentiated cells did not. Our experimental findings indicated that differentiation is important for immortalized cell lines to render post-mitotic neuronal properties, and that differentiated HT22 neurons represent a better model of hippocampal neurons than undifferentiated cells.

Indexed as

brain injurydifferentiationexcitatory neurotoxicityglutamategrants-supported paperhippocampusHT22memantinemitosisMK-801neural regenerationneuronsneuroregenerationN-methyl-D-aspartate receptor

Identifiers

PMID25206424
PMCPMC4107644
OpenAlexW1927624794

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.