Evidence map›Paper›PMID 37471228›Full record

ArticleCell reports2023

Chemogenetic regulation of the TARP-lipid interaction mimics LTP and reversibly modifies behavior.

Joongkyu Park, Coralie Berthoux, Erika Hoyos-Ramirez, Lili Shan, Megumi Morimoto-Tomita, Yixiang Wang, Pablo E Castillo, Susumu Tomita

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 1 country.

Joongkyu ParkDepartment of Cellular and Molecular Physiology, Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Pharmacology, Department of Neurology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Coralie BerthouxDominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Erika Hoyos-RamirezDepartment of Cellular and Molecular Physiology, Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA.
Lili ShanDepartment of Cellular and Molecular Physiology, Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA.
Megumi Morimoto-TomitaDepartment of Cellular and Molecular Physiology, Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA.
Yixiang WangDepartment of Cellular and Molecular Physiology, Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA.
Pablo E CastilloDominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Department of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Susumu TomitaDepartment of Cellular and Molecular Physiology, Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: susumu.tomita@yale.edu.
Yale University · USAlbert Einstein College of Medicine · USWayne State University · US

Funding

Regulation of glutamate receptors by calcium-dependent protein kinasesR01MH077939 · NIMH · YALE UNIVERSITY · PI TOMITA, SUSUMU · 2008 to 2023
$5.2M
Activity-dependent synaptic plasticity expressed by NMDARsR01MH081935 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CASTILLO, PABLO E · 2008 to 2018
$4.0M
Presynaptic forms of long-term plasticity in the CNSR01MH125772 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI PABLO E CASTILLO · 2020 to 2026
$3.6M
Synaptic Mechanisms for Contextual Memory FormationR01MH116673 · NIMH · UPSTATE MEDICAL UNIVERSITY · PI CASTILLO, PABLO E, LIN, YINGXI · 2019 to 2023
$3.4M
Activity-Dependent Plasticity in an Associative Hippocampal Circuit: Mechanisms, Synaptic Learning Rules and Involvement in DiseaseR01NS113600 · NINDS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI CASTILLO, PABLO E · 2019 to 2023
$2.7M
Develop and validate novel chemogenetic tools to modulate synaptic transmissionRF1MH114078 · NIMH · YALE UNIVERSITY · PI TOMITA, SUSUMU · 2017 to 2017
$1.3M
Cell-type-specific and high-resolution profiling of postsynaptic proteomes altered in Alzheimer's disease model miceR21AG068423 · NIA · WAYNE STATE UNIVERSITY · PI PARK, JOONGKYU · 2020 to 2020
$424k
NIA NIH HHS R21 AG068423NIMH NIH HHS R01 MH077939NIMH NIH HHS R01 MH081935NIMH NIH HHS R01 MH116673NIMH NIH HHS R01 MH125772NIMH NIH HHS RF1 MH114078NINDS NIH HHS R01 NS113600
6 · The paper itself

Abstract

Long-term potentiation (LTP), a well-characterized form of synaptic plasticity, is believed to underlie memory formation. Hebbian, postsynaptically expressed LTP requires TARPγ-8 phosphorylation for synaptic insertion of AMPA receptors (AMPARs). However, it is unknown whether TARP-mediated AMPAR insertion alone is sufficient to modify behavior. Here, we report the development of a chemogenetic tool, ExSYTE (Excitatory SYnaptic Transmission modulator by Engineered TARPγ-8), to mimic the cytoplasmic interaction of TARP with the plasma membrane in a doxycycline-dependent manner. We use this tool to examine the specific role of synaptic AMPAR potentiation in amygdala neurons that are activated by fear conditioning. Selective expression of active ExSYTE in these neurons potentiates AMPAR-mediated synaptic transmission in a doxycycline-dependent manner, occludes synaptically induced LTP, and mimics freezing triggered by cued fear conditioning. Thus, chemogenetic controlling of the TARP-membrane interaction is sufficient for LTP-like synaptic AMPAR insertion, which mimics fear conditioning.

Indexed as

DoxycyclineLong-Term PotentiationLipidsNuclear ProteinsSynapsesSynaptic TransmissionDoxycyclineLipidsNuclear ProteinsTARPAMPA receptoramygdalaauxiliary subunitsCaMKIIchemogeneticsCP: Cell biologyCP: Neurosciencefear conditioninglipidphosphorylationsynaptic plasticitysynaptic transmission

Identifiers

PMID37471228
PMCPMC10528344
OpenAlexW4384923080

What OpenQuestion holds

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Registered trials

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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.