Evidence map›Paper›PMID 39225597›Full record

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

Increased GluK1 Subunit Receptors in Corticostriatal Projection from the Anterior Cingulate Cortex Contributed to Seizure-Like Activities.

Xu-Hui Li, Wantong Shi, Zhi-Xia Zhao, Takanori Matsuura, Jing-Shan Lu, Jingmin Che, Qi-Yu Chen, Zhaoxiang Zhou, Man Xue, Shun Hao and 5 more

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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 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

15 authors.

Xu-Hui LiCenter for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, China.ORCID 0000-0003-4376-6252
Wantong ShiCenter for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, China.
Zhi-Xia ZhaoCenter for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, China.
Takanori MatsuuraDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, Ontario, M5S 1A8, Canada.
Jing-Shan LuCenter for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, China.
Jingmin CheShaanxi Provincial Key Laboratory of Infection and Immune Diseases, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China.
Qi-Yu ChenCAS Key Laboratory of Brain Connectome and Manipulation, Interdisciplinary Center for Brain Information, The Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Shenzhen, Guangdong, 518055, China.
Zhaoxiang ZhouDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, Ontario, M5S 1A8, Canada.
Man XueCenter for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, China.
Shun HaoDepartment of Pharmacology, Qingdao University School of Pharmacy, Qingdao, Shandong, 266071, China.
Fang XuCAS Key Laboratory of Brain Connectome and Manipulation, Interdisciplinary Center for Brain Information, The Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Shenzhen, Guangdong, 518055, China.
Guo-Qiang BiCAS Key Laboratory of Brain Connectome and Manipulation, Interdisciplinary Center for Brain Information, The Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Shenzhen, Guangdong, 518055, China.
Bong-Kiun KaangDepartment of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul, 151-746, South Korea.
Graham L CollingridgeDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, Ontario, M5S 1A8, Canada.
Min ZhuoCenter for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, China.ORCID 0000-0001-9062-3241

Funding

4/5: Antipsychotic Response to Clozapine in B-SNIP Biotype-1 (CLOZAPINE)R01MH124807 · NIMH · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KESHAVAN, MATCHERI S. · 2021 to 2025
$1.4M
EJLB-CIHR Michael Smith Chair in Neurosciences and Mental Health in Canada, Canada Research Chair, Ontario-China Research and Innovation Fund (OCRIF), Canadian Institute for Health Research operating and project Grants 4192864EJLB-CIHR Michael Smith Chair in Neurosciences and Mental Health in Canada, Canada Research Chair, Ontario-China Research and Innovation Fund (OCRIF), Canadian Institute for Health Research operating and project Grants MOP-124807EJLB-CIHR Michael Smith Chair in Neurosciences and Mental Health in Canada, Canada Research Chair, Ontario-China Research and Innovation Fund (OCRIF), Canadian Institute for Health Research operating and project Grants PJT-148648Fundamental Research Funds for the Central Universities xxj032022013Fundamental Research Funds for the Central Universities xzy012022046National Honor Scientist Program of Korea NRF-2012R1A3A1050385National Natural Science Foundation of China 32100810
6 · The paper itself

Abstract

The corticostriatal connection plays a crucial role in cognitive, emotional, and motor control. However, the specific roles and synaptic transmissions of corticostriatal connection are less studied, especially the corticostriatal transmission from the anterior cingulate cortex (ACC). Here, a direct glutamatergic excitatory synaptic transmission in the corticostriatal projection from the ACC is found. Kainate receptors (KAR)-mediated synaptic transmission is increased in this corticostriatal connection both in vitro and in vivo seizure-like activities. GluK1 containing KARs and downstream calcium-stimulated adenylyl cyclase subtype 1 (AC1) are involved in the upregulation of KARs following seizure-like activities. Inhibiting the activities of ACC or its corticostriatal connection significantly attenuated pentylenetetrazole (PTZ)-induced seizure. Additionally, injection of GluK1 receptor antagonist UBP310 or the AC1 inhibitor NB001 both show antiepileptic effects. The studies provide direct evidence that KARs are involved in seizure activity in the corticostriatal connection and the KAR-AC1 signaling pathway is a potential novel antiepileptic strategy.

Indexed as

Gyrus CinguliKainic Acid ReceptorsSeizuresAnimalsCorpus StriatumDisease Models, AnimalMaleMiceMice, Inbred C57BLPentylenetetrazoleSynaptic TransmissionKainic Acid ReceptorsPentylenetetrazoleAC1anterior cingulate cortexcorticostriatal projectionkainate receptorseizurestriatum

Identifiers

PMID39225597
PMCPMC11497107

What OpenQuestion holds

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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 OpenQuestion graph.