Evidence map›Paper›PMID 23616545›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Multiple sources of striatal inhibition are differentially affected in Huntington's disease mouse models.

Carlos Cepeda, Laurie Galvan, Sandra M Holley, Shilpa P Rao, Véronique M André, Elian P Botelho, Jane Y Chen, Joseph B Watson, Karl Deisseroth, Michael S Levine

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
3.9field-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

84 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Restoring Compromised ClThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Article
  9. Bioengineering & translational medicine · 2024
    Article
  10. Application of Optogenetics in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2024
    Review
  11. Transplanted human neural stem cells rescue phenotypes in zQ175 Huntington's disease mice and innervate the striatum.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Astrocytic contributions to Huntington's disease pathophysiology.Annals of the New York Academy of Sciences · 2023
    Review
  16. Article
  17. Article
  18. Bayesian Mapping of the Striatal Microcircuit Reveals Robust Asymmetries in the Probabilities and Distances of Connections.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  19. Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022
    Article
  20. Cannabinoid signaling and risk in Huntington's disease.Frontiers in computational neuroscience · 2022
    Article

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

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

10 authors at 3 institutions in 1 country.

Carlos CepedaIntellectual and Developmental Disabilities Research Center, Brain Research Institute, Semel Institute for Neuroscience, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA.
Laurie Galvan
Sandra M Holley
Shilpa P Rao
Véronique M André
Elian P Botelho
Jane Y Chen
Joseph B Watson
Karl Deisseroth
Michael S Levine
University of California, Los Angeles · USAllen Institute for Brain Science · USStanford University · US

Funding

Transgenic Mouse Models of Huntington's DiseaseR01NS041574 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEVINE, MICHAEL S. · 2002 to 2016
$5.4M
NINDS NIH HHS NS 41574NINDS NIH HHS R01 NS041574
6 · The paper itself

Abstract

In Huntington's disease (HD) mouse models, spontaneous inhibitory synaptic activity is enhanced in a subpopulation of medium-sized spiny neurons (MSNs), which could dampen striatal output. We examined the potential source(s) of increased inhibition using electrophysiological and optogenetic methods to assess feedback and feedforward inhibition in two transgenic mouse models of HD. Single whole-cell patch-clamp recordings demonstrated that increased GABA synaptic activity impinges principally on indirect pathway MSNs. Dual patch recordings between MSNs demonstrated reduced connectivity between MSNs in HD mice. However, while connectivity was strictly unidirectional in controls, in HD mice bidirectional connectivity occurred. Other sources of increased GABA activity in MSNs also were identified. Dual patch recordings from fast spiking (FS) interneuron-MSN pairs demonstrated greater but variable amplitude responses in MSNs. In agreement, selective optogenetic stimulation of parvalbumin-expressing, FS interneurons induced significantly larger amplitude MSN responses in HD compared with control mice. While there were no differences in responses of MSNs evoked by activating single persistent low-threshold spiking (PLTS) interneurons in recorded pairs, these interneurons fired more action potentials in both HD models, providing another source for increased frequency of spontaneous GABA synaptic activity in MSNs. Selective optogenetic stimulation of somatostatin-expressing, PLTS interneurons did not reveal any significant differences in responses of MSNs in HD mice. These findings provide strong evidence that both feedforward and to a lesser extent feedback inhibition to MSNs in HD can potentially be sources for the increased GABA synaptic activity of indirect pathway MSNs.

Indexed as

Disease Models, AnimalAction PotentialsAnimalsCorpus StriatumFemaleHumansHuntington DiseaseMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicNeural Inhibition

Identifiers

PMID23616545
PMCPMC3686572
OpenAlexW2082078838

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.