Evidence map›Paper›PMID 28334608›Full record

ArticleNeuron2017

Parvalbumin Interneurons Modulate Striatal Output and Enhance Performance during Associative Learning.

Kwang Lee, Sandra M Holley, Justin L Shobe, Natalie C Chong, Carlos Cepeda, Michael S Levine, Sotiris C Masmanidis

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Neuron, 2017. 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 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
19.4field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 139 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Kwang LeeDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Sandra M HolleyIntellectual and Developmental Disabilities Research Center, Brain Research Institute, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Justin L ShobeDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Natalie C ChongNeuroscience Interdepartmental Program, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Carlos CepedaIntellectual and Developmental Disabilities Research Center, Brain Research Institute, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Michael S LevineIntellectual and Developmental Disabilities Research Center, Brain Research Institute, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Sotiris C MasmanidisDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; California Nanosystems Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA; Brain Research Institute, Integrative Center for Learning and Memory, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: smasmanidis@ucla.edu.
University of California, Los Angeles · USCalifornia NanoSystems Institute · US

Funding

UCLA Center for Translational Research in Neurodevelopment: UC-TRaNU54HD087101 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MCCRACKEN, JAMES T. · 2016 to 2020
$6.5M
Transgenic Mouse Models of Huntington's DiseaseR01NS041574 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEVINE, MICHAEL S. · 2002 to 2016
$5.4M
Systems-level electrophysiology for addiction and reward researchR01DA034178 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MASMANIDIS, SOTIRIS · 2012 to 2016
$1.5M
CRCNS: Network mechanisms of the learning and encoding of timed motor responsesR01NS100050 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BUONOMANO, DEAN V, MASMANIDIS, SOTIRIS · 2016 to 2020
$1.5M
NICHD NIH HHS U54 HD087101NIDA NIH HHS R01 DA034178NINDS NIH HHS R01 NS041574NINDS NIH HHS R01 NS100050
6 · The paper itself

Abstract

The prevailing view is that striatal parvalbumin (PV)-positive interneurons primarily function to downregulate medium spiny projection neuron (MSN) activity via monosynaptic inhibitory signaling. Here, by combining in vivo neural recordings and optogenetics, we unexpectedly find that both suppressing and over-activating PV cells attenuates spontaneous MSN activity. To account for this, we find that, in addition to monosynaptic coupling, PV-MSN interactions are mediated by a competing disynaptic inhibitory circuit involving a variety of neuropeptide Y-expressing interneurons. Next we use optogenetic and chemogenetic approaches to show that dorsolateral striatal PV interneurons influence the initial expression of reward-conditioned responses but that their contribution to performance declines with experience. Consistent with this, we observe with large-scale recordings in behaving animals that the relative contribution of PV cells on MSN activity diminishes with training. Together, this work provides a possible mechanism by which PV interneurons modulate striatal output and selectively enhance performance early in learning.

Indexed as

Action PotentialsAnimalsAssociation LearningCorpus StriatumInterneuronsMiceMice, TransgenicNeural InhibitionNeuropeptide YParvalbuminsRewardNeuropeptide YParvalbuminsdisynaptic inhibitionlearningneural recordingoptogeneticsparvalbumin interneuronsreward conditioningstriatum

Identifiers

PMID28334608
PMCPMC5386608
OpenAlexW2602352603

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.