Evidence map›Paper›PMID 29691329›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

Striatal Direct and Indirect Pathway Output Structures Are Differentially Altered in Mouse Models of Huntington's Disease.

Joshua Barry, Garnik Akopian, Carlos Cepeda, Michael S Levine

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Restoring Compromised ClThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Application of Optogenetics in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2024
    Review
  7. Leucine-rich repeat kinase 2 limits dopamine D1 receptor signaling in striatum and biases against heavy persistent alcohol drinking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
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  18. Article
  19. Article
  20. New era of optogenetics: from the central to peripheral nervous system.Critical reviews in biochemistry and molecular biology · 2020
    Review
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

4 authors at 2 institutions in 1 country.

Joshua BarryIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, Brain Research Institute, University of California-Los Angeles, Los Angeles, California 90095.
Garnik AkopianIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, Brain Research Institute, University of California-Los Angeles, Los Angeles, California 90095.
Carlos CepedaIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, Brain Research Institute, University of California-Los Angeles, Los Angeles, California 90095.ORCID 0000-0001-5953-6692
Michael S LevineIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, Brain Research Institute, University of California-Los Angeles, Los Angeles, California 90095 mlevine@mednet.ucla.edu.ORCID 0000-0001-8681-204X
Allen Institute for Brain Science · USUniversity of California, Los Angeles · US

Funding

UCLA Center for Translational Research in Neurodevelopment: UC-TRaNU54HD087101 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOOKHEIMER, SUSAN Y · 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
Optogenetic Stimulation of Striatal Output Neurons in Mouse Models of Huntingtons DiseaseF32NS093813 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BARRY, JOSHUA · 2016 to 2018
$183k
NICHD NIH HHS U54 HD087101NINDS NIH HHS F32 NS093813NINDS NIH HHS R01 NS041574
6 · The paper itself

Abstract

The present study examined synaptic communication between direct and indirect output pathway striatal medium-sized spiny neurons (MSNs) and their target structures, the substantia nigra pars reticulata (SNr) and the external globus pallidus (GPe) in two mouse models of Huntington's disease (HD). Cre recombination, optogenetics, and whole-cell patch-clamp recordings were used to determine alterations in intrinsic and synaptic properties of SNr and GPe neurons from both male and female symptomatic R6/2 (>60 d) and presymptomatic (2 months) or symptomatic (10-12 months) YAC128 mice. Cell membrane capacitance was decreased, whereas input resistance was increased in SNr neurons from R6/2, but not YAC128 mice. The amplitude of GABAergic responses evoked by optogenetic stimulation of direct pathway terminals was reduced in SNr neurons of symptomatic mice of both models. A decrease in spontaneous GABA synaptic activity, in particular large-amplitude events, in SNr neurons also was observed. Passive membrane properties of GPe neurons were not different between R6/2 or YAC128 mice and their control littermates. Similarly, the amplitude of GABA responses evoked by activation of indirect pathway MSN terminals and the frequency of spontaneous GABA synaptic activity were similar in HD and control animals. In contrast, the decay time of the evoked GABA response was significantly longer in cells from HD mice. Interestingly, activation of indirect pathway MSNs within the striatum evoked larger-amplitude responses in direct pathway MSNs. Together, these results demonstrate differential alterations in responses evoked by direct and indirect pathway terminals in SNr and GPe leading to striatal output imbalance and motor dysfunction.

Indexed as

AnimalsCell CommunicationCell MembraneCorpus StriatumElectrophysiological PhenomenaExcitatory Postsynaptic PotentialsFemaleGABA Agonistsgamma-Aminobutyric AcidGlobus PallidusHuntington DiseaseMaleMiceNeural PathwaysNeuronsOptogeneticsGABA Agonistsgamma-Aminobutyric Acidelectrophysiologyexternal globus pallidusHuntington's diseaseoptogeneticssubstantia nigrasynaptic activity

Identifiers

PMID29691329
PMCPMC5956986
OpenAlexW2801531716

What OpenQuestion holds

Textmetadata
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.