Evidence map›Paper›PMID 28176786›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2017

Disrupted Glutamatergic Transmission in Prefrontal Cortex Contributes to Behavioral Abnormality in an Animal Model of ADHD.

Jia Cheng, Aiyi Liu, Michael Y Shi, Zhen Yan

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 72 citations in OpenAlex.

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  15. Role of Glutamate Receptor-related Biomarkers in the Etiopathogenesis of ADHD.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024
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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

4 authors at 1 institution in 1 country.

Jia ChengDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY, USA.
Aiyi LiuDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY, USA.
Michael Y ShiDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY, USA.
Zhen YanDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY, USA.
University at Buffalo, State University of New York · US

Funding

Physiological and Pathophysiological Basis of StressR01MH108842 · NIMH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YAN, ZHEN · 2015 to 2019
$2.0M
Functions of D4 Dopamine Receptors in Prefrontal CortexR01DA037618 · NIDA · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YAN, ZHEN · 2014 to 2018
$1.7M
NIDA NIH HHS R01 DA037618NIMH NIH HHS R01 MH108842
6 · The paper itself

Abstract

Spontaneously hypertensive rats (SHR) are the most widely used animal model for the study of attention deficit hyperactivity disorder (ADHD). Here we sought to reveal the neuronal circuits and molecular basis of ADHD and its potential treatment using SHR. Combined electrophysiological, biochemical, pharmacological, chemicogenetic, and behavioral approaches were utilized. We found that AMPAR-mediated synaptic transmission in pyramidal neurons of prefrontal cortex (PFC) was diminished in SHR, which was correlated with the decreased surface expression of AMPAR subunits. Administration of methylphenidate (a psychostimulant drug used to treat ADHD), which blocks dopamine transporters and norepinephrine transporters, ameliorated the behavioral deficits of adolescent SHR and restored AMPAR-mediated synaptic function. Activation of PFC pyramidal neurons with a CaMKII-driven Gq-coupled designer receptor exclusively activated by designer drug also led to the elevation of AMPAR function and the normalization of ADHD-like behaviors in SHR. These results suggest that the disrupted function of AMPARs in PFC may underlie the behavioral deficits in adolescent SHR and enhancing PFC activity could be a treatment strategy for ADHD.

Indexed as

AnimalsAttention Deficit Disorder with HyperactivityCentral Nervous System StimulantsDisease Models, AnimalGlutamic AcidMaleMethylphenidatePrefrontal CortexPyramidal CellsRats, Inbred SHRRats, Sprague-DawleyRats, WistarReceptors, AMPAReceptors, N-Methyl-D-AspartateSynaptic TransmissionCentral Nervous System StimulantsGlutamic AcidMethylphenidateReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID28176786
PMCPMC5561342
OpenAlexW2587060638

What OpenQuestion holds

Textmetadata
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.