Evidence map›Paper›PMID 35494226›Full record

ArticleiScience2022

Paradoxical effects of posterior intralaminar thalamic calretinin neurons on hippocampal seizure via distinct downstream circuits.

Yingbei Qi, Heming Cheng, Qiuwen Lou, Xia Wang, Nanxi Lai, Chenshu Gao, Shuangshuang Wu, Cenglin Xu, Yeping Ruan, Zhong Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Yingbei QiInstitute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Heming ChengKey Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Qiuwen LouKey Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Xia WangInstitute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Nanxi LaiInstitute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Chenshu GaoKey Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Shuangshuang WuKey Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Cenglin XuKey Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Yeping RuanKey Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Zhong ChenInstitute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Yi WangInstitute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Zhejiang Chinese Medical University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is a circuit-level brain disorder characterized by hyperexcitatory seizures with unclear mechanisms. Here, we investigated the causal roles of calretinin (CR) neurons in the posterior intralaminar thalamic nucleus (PIL) in hippocampal seizures. Using c-fos mapping and calcium fiber photometry, we found that PIL CR neurons were activated during hippocampal seizures in a kindling model. Optogenetic activation of PIL CR neurons accelerated seizure development, whereas inhibition retarded seizure development. Further, viral-based circuit tracing verified that PIL CR neurons were long-range glutamatergic neurons, projecting toward various downstream regions. Interestingly, selective inhibition of PIL-lateral amygdala CR circuit attenuated seizure progression, whereas inhibition of PIL-zona incerta CR circuit presented an opposite effect. These results indicated that CR neurons in the PIL play separate roles in hippocampal seizures via distinct downstream circuits, which complements the pathogenic mechanisms of epilepsy and provides new insight for the precise medicine of epilepsy.

Indexed as

Biological sciencesCellular neuroscienceMolecular neuroscience

Identifiers

PMID35494226
PMCPMC9046245
OpenAlexW4225300186

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.