Evidence map›Paper›PMID 26833136›Full record

ArticleNeuron2016

Pathway-Specific Remodeling of Thalamostriatal Synapses in Parkinsonian Mice.

Philip R L Parker, Arnaud L Lalive, Anatol C Kreitzer

Abstract read
In one paragraph

Article in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing 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

72 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Dysfunction of motor cortices in Parkinson's disease.Cerebral cortex (New York, N.Y. : 1991) · 2024
    Review
  12. Article
  13. Article
  14. Imaging-based chemogenetics for dissecting neural circuits in nonhuman primates.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2024
    Review
  15. Review
  16. Article
  17. Altered Thalamocortical Signaling in a Mouse Model of Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Philip R L ParkerNeuroscience Graduate Program, University of California, San Francisco, San Francisco, CA 94143, USA; Gladstone Institutes, San Francisco, CA 94158, USA.
Arnaud L LaliveGladstone Institutes, San Francisco, CA 94158, USA.
Anatol C KreitzerNeuroscience Graduate Program, University of California, San Francisco, San Francisco, CA 94143, USA; Gladstone Institutes, San Francisco, CA 94158, USA; Departments of Physiology and Neurology, University of California San Francisco, CA 94158, USA. Electronic address: akreitzer@gladstone.ucsf.edu.

Funding

Neuron- and Circuit-Specific Mechanisms and Adaptations Regulating Striatal FunctR01NS064984 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI KREITZER, ANATOL · 2009 to 2022
$5.1M
Striatal Microcircuits: Regulation and FunctionR01NS078435 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BERKE, JOSHUA D, KREITZER, ANATOL · 2012 to 2016
$2.4M
Thalamostriatal pathophysiology in Parkinson's diseaseF31NS080543 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PARKER, PHILIP ROSS LUTTON · 2012 to 2014
$93k
NINDS NIH HHS 1F31NS080543NINDS NIH HHS F31 NS080543NINDS NIH HHS NIH R01 NS064984NINDS NIH HHS R01 NS064984NINDS NIH HHS R01 NS078435
6 · The paper itself

Abstract

Movement suppression in Parkinson's disease (PD) is thought to arise from increased efficacy of the indirect pathway basal ganglia circuit, relative to the direct pathway. However, the underlying pathophysiological mechanisms remain elusive. To examine whether changes in the strength of synaptic inputs to these circuits contribute to this imbalance, we obtained paired whole-cell recordings from striatal direct- and indirect-pathway medium spiny neurons (dMSNs and iMSNs) and optically stimulated inputs from sensorimotor cortex or intralaminar thalamus in brain slices from control and dopamine-depleted mice. We found that dopamine depletion selectively decreased synaptic strength at thalamic inputs to dMSNs, suggesting that thalamus drives asymmetric activation of basal ganglia circuitry underlying parkinsonian motor impairments. Consistent with this hypothesis, in vivo chemogenetic and optogenetic inhibition of thalamostriatal terminals reversed motor deficits in dopamine-depleted mice. These results implicate thalamostriatal projections in the pathophysiology of PD and support interventions targeting thalamus as a potential therapeutic strategy.

Indexed as

Adrenergic Agentsalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsCorpus StriatumDisease Models, AnimalEmpty Spiracles Homeobox ProteinsExcitatory Amino Acid AgonistsExcitatory Postsynaptic PotentialsExploratory BehaviorFunctional LateralityHomeodomain ProteinsMedial Forebrain BundleMiceNeural PathwaysN-MethylaspartateOxidopamineAdrenergic Agentsalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidEmpty Spiracles Homeobox ProteinsExcitatory Amino Acid AgonistsHomeodomain ProteinsN-MethylaspartateOxidopamineSlc17a6 protein, mouseTranscription FactorsTyrosine 3-MonooxygenaseVesicular Glutamate Transport Protein 2

Identifiers

PMID26833136
PMCPMC4760843

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.