Evidence map›Paper›PMID 25070512›Full record

ArticleBrain : a journal of neurology2014

Response inhibition and serotonin in autism: a functional MRI study using acute tryptophan depletion.

Eileen Daly, Christine Ecker, Brian Hallahan, Quinton Deeley, Michael Craig, Clodagh Murphy, Patrick Johnston, Debbie Spain, Nicola Gillan, Maria Gudbrandsen and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 4 pooled it
4.1field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 4 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  5. Trial
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  8. Autism and Cortical Thickness Deviation From Neurotypical Controls: Evidence for a Spatial Association With Serotonin Receptors.Autism research : official journal of the International Society for Autism Research · 2026
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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

20 authors at 6 institutions in 3 countries.

Eileen Daly1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK eileen.daly@kcl.ac.uk.
Christine Ecker1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Brian Hallahan2 Department of Psychiatry, National University of Ireland, Galway, Ireland.
Quinton Deeley1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Michael Craig1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Clodagh Murphy1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Patrick Johnston1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Debbie Spain1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Nicola Gillan1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Maria Gudbrandsen1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Michael Brammer3 Department of Neuroimaging, Institute of Psychiatry, King's College London, UK.
Vincent Giampietro3 Department of Neuroimaging, Institute of Psychiatry, King's College London, UK.
Melissa Lamar4 Department of Psychiatry, University of Illinois at Chicago, USA.
Lisa Page5 Sussex Partnership NHS Foundation Trust, Brighton and Sussex Medical School, Brighton, UK.
Fiona Toal1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
Nicole Schmitz6 Dementia Research Unit, Institute of Neurology, University College London, UK.
Anthony Cleare7 Department of Psychological Medicine, Institute of Psychiatry, King's College London, UK.
Dene Robertson8 Behavioural and Developmental Clinical Academic Group, South London and Maudsley NHS Foundation.
Katya Rubia9 Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London, UK.
Declan G M Murphy1 Sackler Institute of Translational Neurodevelopment, Department of Forensic and Neurodevelopmental Science, Institute of Psychiatry, King's College London, UK.
King's College London · GBOllscoil na Gaillimhe – University of Galway · IESouth London and Maudsley NHS Foundation Trust · GBSussex Partnership NHS Foundation Trust · GBUK Dementia Research Institute · GBUniversity of Illinois Chicago · US

Funding

Department of Health CDRF-2012-03-059Department of Health RP-PG-0606-1045Medical Research Council G0400061
6 · The paper itself

Abstract

It has been suggested that the restricted, stereotyped and repetitive behaviours typically found in autism are underpinned by deficits of inhibitory control. The biological basis of this is unknown but may include differences in the modulatory role of neurotransmitters, such as serotonin, which are implicated in the condition. However, this has never been tested directly. We therefore assessed the modifying role of serotonin on inhibitory brain function during a Go/No-Go task in 14 adults with autism and normal intelligence and 14 control subjects that did not differ in gender, age and intelligence. We undertook a double-blind, placebo-controlled, crossover trial of acute tryptophan depletion using functional magnetic resonance imaging. Following sham, adults with autism relative to controls had reduced activation in key inhibitory regions of inferior frontal cortex and thalamus, but increased activation of caudate and cerebellum. However, brain activation was modulated in opposite ways by depletion in each group. Within autistic individuals depletion upregulated fronto-thalamic activations and downregulated striato-cerebellar activations toward control sham levels, completely 'normalizing' the fronto-cerebellar dysfunctions. The opposite pattern occurred in controls. Moreover, the severity of autism was related to the degree of differential modulation by depletion within frontal, striatal and thalamic regions. Our findings demonstrate that individuals with autism have abnormal inhibitory networks, and that serotonin has a differential, opposite, effect on them in adults with and without autism. Together these factors may partially explain the severity of autistic behaviours and/or provide a novel (tractable) treatment target.

Indexed as

Magnetic Resonance ImagingAdolescentAdultAutistic DisorderBrainCross-Over StudiesDouble-Blind MethodFemaleHumansMaleNeural InhibitionPhotic StimulationReaction TimeSerotoninTryptophanYoung AdultSerotoninTryptophanautistic spectrum disorderimpulsivity and inhibition disorders

Identifiers

PMID25070512
PMCPMC4132649
OpenAlexW1980484880

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.