Evidence map›Paper›PMID 31678398›Full record

ArticleNeuropharmacology2020

Alcohol exposure in utero disrupts cortico-striatal coordination required for behavioral flexibility.

Kristin Marquardt, James F Cavanagh, Jonathan L Brigman

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 33 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kristin MarquardtDepartment of Neurosciences, University of New Mexico School of Medicine, Albuquerque, NM, USA.
James F CavanaghDepartment of Psychology, University of New Mexico, Albuquerque, NM, USA.
Jonathan L BrigmanDepartment of Neurosciences, University of New Mexico School of Medicine, Albuquerque, NM, USA; New Mexico Alcohol Research Center, UNM Health Sciences Center, Albuquerque, NM, USA. Electronic address: jbrigman@salud.unm.edu.
University of New Mexico · US

Funding

Understanding neurophysiological deficits in response inhibition in children with FASDP50AA022534 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2014 to 2026
$21.5M
Alcohol Research Training in NeurosciencesT32AA014127 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Jonathan L Brigman · 2003 to 2026
$3.3M
Prenatal alcohol exposure and corticostriatal mediation of behavioral flexibilityR01AA025652 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BRIGMAN, JONATHAN L · 2018 to 2022
$1.7M
Altered neuronal dynamics of executive control after prenatal alcohol exposureF31AA025259 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI MARQUARDT, KRISTIN LEE · 2016 to 2016
$44k
NIAAA NIH HHS F31 AA025259NIAAA NIH HHS P50 AA022534NIAAA NIH HHS R01 AA025652NIAAA NIH HHS T32 AA014127
6 · The paper itself

Abstract

Deficits in behavioral flexibility are a hallmark of multiple psychiatric, neurological, and substance use disorders. These deficits are often marked by decreased function of the prefrontal cortex (PFC); however, the genesis of such executive deficits remains understudied. Here we report how the most preventable cause of developmental disability, in utero exposure to alcohol, alters cortico-striatal circuit activity leading to impairments in behavioral flexibility in adulthood. We utilized a translational touch-screen task coupled with in vivo electrophysiology in adult mice to examine single unit and coordinated activity of the lateral orbital frontal cortex (OFC) and dorsolateral striatum (DS) during flexible behavior. Prenatal alcohol exposure (PAE) decreased OFC, and increased DS, single unit activity during reversal learning and altered the number of choice responsive neurons in both regions. PAE also decreased coordinated activity within the OFC and DS as measured by oscillatory field activity and altered spike-field coupling. Furthermore, PAE led to sustained connectivity between regions past what was seen in control animals. These findings suggest that PAE causes altered coordination within and between the OFC and DS, promoting maladaptive perseveration. Our model suggests that in optimally functioning mice OFC disengages the DS and updates the newly changed reward contingency, whereas in PAE animals, aberrant and persistent OFC to DS signaling drives behavioral inflexibility during early reversal sessions. Together, these findings demonstrate how developmental exposure alters circuit-level activity leading to behavioral deficits and suggest a critical role for coordination of neural timing during behaviors requiring executive function.

Indexed as

Action PotentialsAdaptation, PsychologicalAnimalsCentral Nervous System DepressantsCerebral CortexConditioning, OperantDiscrimination LearningElectrodiagnosisEthanolExecutive FunctionFemaleMaleMiceNeostriatumNeural PathwaysPrefrontal CortexCentral Nervous System DepressantsEthanolExecutive controlIn vivo electrophysiologyLocal field potentialTouchscreen

Identifiers

PMID31678398
PMCPMC6899166
OpenAlexW2985804038

What OpenQuestion holds

Textmetadata
LicenceTDM
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.