Evidence map›Paper›PMID 30295606›Full record

ArticleeLife2018

Motor thalamus supports striatum-driven reinforcement.

Arnaud L Lalive, Anthony D Lien, Thomas K Roseberry, Christopher H Donahue, Anatol C Kreitzer

Abstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Optogenetic Stimulation of Novel Tph2-Cre Rats Advances Insight into Serotonin's Role in Locomotion, Reinforcement, and Compulsivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Operant self-stimulation of thalamic terminals in the dorsomedial striatum is constrained by metabotropic glutamate receptor 2.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Article
  13. Review
  14. Article
  15. Circuits That Mediate Expression of Signaled Active Avoidance Converge in the Pedunculopontine Tegmentum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  16. Article
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

5 authors.

Arnaud L LaliveThe Gladstone Institutes, San Francisco, United States.
Anthony D LienThe Gladstone Institutes, San Francisco, United States.
Thomas K RoseberryThe Gladstone Institutes, San Francisco, United States.
Christopher H DonahueThe Gladstone Institutes, San Francisco, United States.
Anatol C KreitzerThe Gladstone Institutes, San Francisco, United States.ORCID http://orcid.org/0000-0001-7423-2398

Funding

The Presynaptic Vesicle Cycle for the Slow Acting Neurotransmitter SecretionP01DA010154 · NIDA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EDWARDS, ROBERT H, KREITZER, ANATOL · 1995 to 2016
$14.7M
Neuron- and Circuit-Specific Mechanisms and Adaptations Regulating Striatal FunctR01NS064984 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI KREITZER, ANATOL · 2009 to 2022
$5.1M
Network basis of action selectionU01NS094342 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI KOMIYAMA, TAKAKI, KREITZER, ANATOL · 2015 to 2017
$3.0M
NIDA NIH HHS P01 DA010154NIH HHS P01 DA010154NIH HHS R01 NS064984NIH HHS U01 NS094342NINDS NIH HHS R01 NS064984NINDS NIH HHS U01 NS094342
6 · The paper itself

Abstract

Reinforcement has long been thought to require striatal synaptic plasticity. Indeed, direct striatal manipulations such as self-stimulation of direct-pathway projection neurons (dMSNs) are sufficient to induce reinforcement within minutes. However, it's unclear what role, if any, is played by downstream circuitry. Here, we used dMSN self-stimulation in mice as a model for striatum-driven reinforcement and mapped the underlying circuitry across multiple basal ganglia nuclei and output targets. We found that mimicking the effects of dMSN activation on downstream circuitry, through optogenetic suppression of basal ganglia output nucleus substantia nigra reticulata (SNr) or activation of SNr targets in the brainstem or thalamus, was also sufficient to drive rapid reinforcement. Remarkably, silencing motor thalamus-but not other selected targets of SNr-was the only manipulation that reduced dMSN-driven reinforcement. Together, these results point to an unexpected role for basal ganglia output to motor thalamus in striatum-driven reinforcement.

Indexed as

Reinforcement, PsychologyAnimalsBasal GangliaElectric StimulationFemaleGlutamatesMaleMiceMotor ActivityNeostriatumOptogeneticsReceptors, N-Methyl-D-AspartateSerotonergic NeuronsSynaptic TransmissionThalamusGlutamatesReceptors, N-Methyl-D-Aspartatemouseneuroscienceoptogeneticsreinforcementstriatum

Identifiers

PMID30295606
PMCPMC6181560

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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.