Evidence map›Paper›PMID 38670100›Full record

ArticleCell reports. Medicine2024

Restoring thalamocortical circuit dysfunction by correcting HCN channelopathy in Shank3 mutant mice.

Baolin Guo, Tiaotiao Liu, Soonwook Choi, Honghui Mao, Wenting Wang, Kaiwen Xi, Carter Jones, Nolan D Hartley, Dayun Feng, Qian Chen and 15 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
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

25 authors at 6 institutions in 2 countries.

Baolin GuoDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Tiaotiao LiuSchool of Biomedical Engineering and Technology, Tianjin Medical University, Tianjin 300070, China.
Soonwook ChoiStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA.
Honghui MaoDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Wenting WangDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Kaiwen XiDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Carter JonesStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Nolan D HartleyStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA.
Dayun FengDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Qian ChenMcGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA.
Yingying LiuDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Ralf D WimmerMcGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA.
Yuqiao XieDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Ningxia ZhaoXi'an TCM Hospital of Encephalopathy, Shaanxi University of Chinese Medicine, Xi'an 710032, China.
Jianjun OuDepartment of Psychiatry, The Second Xiangya Hospital of Central South University, National Clinical Research Center for Mental Disorders, Changsha 410011, China.
Mario A Arias-GarciaStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Diya MalhotraStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Yang LiuDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Sihak LeeStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Sammuel PasqualoniStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Ryan J KastStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA.
Morgan FleishmanStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Michael M HalassaMcGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA.
Shengxi WuDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China. Electronic address: shengxi@fmmu.edu.cn.
Zhanyan FuStanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA. Electronic address: zfu@broadinstitute.org.
Broad Institute · USAir Force Medical University · CNMcGovern Institute for Brain Research · USSecond Xiangya Hospital of Central South University · CNShaanxi University of Chinese Medicine · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thalamocortical (TC) circuits are essential for sensory information processing. Clinical and preclinical studies of autism spectrum disorders (ASDs) have highlighted abnormal thalamic development and TC circuit dysfunction. However, mechanistic understanding of how TC dysfunction contributes to behavioral abnormalities in ASDs is limited. Here, our study on a Shank3 mouse model of ASD reveals TC neuron hyperexcitability with excessive burst firing and a temporal mismatch relationship with slow cortical rhythms during sleep. These TC electrophysiological alterations and the consequent sensory hypersensitivity and sleep fragmentation in Shank3 mutant mice are causally linked to HCN2 channelopathy. Restoring HCN2 function early in postnatal development via a viral approach or lamotrigine (LTG) ameliorates sensory and sleep problems. A retrospective case series also supports beneficial effects of LTG treatment on sensory behavior in ASD patients. Our study identifies a clinically relevant circuit mechanism and proposes a targeted molecular intervention for ASD-related behavioral impairments.

Indexed as

Autism Spectrum DisorderHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsNerve Tissue ProteinsThalamusAnimalsCerebral CortexChannelopathiesDisease Models, AnimalFemaleHumansLamotrigineMaleMiceMice, Inbred C57BLMicrofilament ProteinsMutationHcn2 protein, mouseHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsLamotrigineMicrofilament ProteinsNerve Tissue ProteinsPotassium ChannelsShank3 protein, mouseASDsautism spectrum disordersHCN2lamotrigineneurodevelopmental disordersShank3sleep fragmentationtactile hypersensitivitythalamocortical circuits

Identifiers

PMID38670100
PMCPMC11149412
OpenAlexW4395450673

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.