Evidence map›Paper›PMID 24920627›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Cerebellar zonal patterning relies on Purkinje cell neurotransmission.

Joshua J White, Marife Arancillo, Trace L Stay, Nicholas A George-Jones, Sabrina L Levy, Detlef H Heck, Roy V Sillitoe

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

69 citing papers in PubMed, 105 citations in OpenAlex.

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  6. Thalamic deep brain stimulation improves movement in a cerebellar model of lesion-based status dystonicus.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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9 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

7 authors at 4 institutions in 1 country.

Joshua J WhiteDepartments of Pathology and Immunology and Department of Neuroscience, Baylor College of Medicine, Jan and Dan Duncan Neurological Research Institute of Texas Children's Hospital, Houston, Texas 77030 and.
Marife ArancilloDepartments of Pathology and Immunology and Department of Neuroscience, Baylor College of Medicine, Jan and Dan Duncan Neurological Research Institute of Texas Children's Hospital, Houston, Texas 77030 and.
Trace L StayDepartments of Pathology and Immunology and Department of Neuroscience, Baylor College of Medicine, Jan and Dan Duncan Neurological Research Institute of Texas Children's Hospital, Houston, Texas 77030 and.
Nicholas A George-JonesDepartments of Pathology and Immunology and Department of Neuroscience, Baylor College of Medicine, Jan and Dan Duncan Neurological Research Institute of Texas Children's Hospital, Houston, Texas 77030 and.
Sabrina L LevyDepartments of Pathology and Immunology and Department of Neuroscience, Baylor College of Medicine, Jan and Dan Duncan Neurological Research Institute of Texas Children's Hospital, Houston, Texas 77030 and.
Detlef H HeckUniversity of Tennessee Health Science Center, Departments of Anatomy and Neurobiology, Memphis, Tennessee 38163.
Roy V SillitoeDepartments of Pathology and Immunology and Department of Neuroscience, Baylor College of Medicine, Jan and Dan Duncan Neurological Research Institute of Texas Children's Hospital, Houston, Texas 77030 and sillitoe@bcm.edu.
Baylor College of Medicine · USNeurological Research Institute · USTexas Children's Hospital · USUniversity of Tennessee Health Science Center · US

Funding

UNDERSTANDING FXTAS AMONG MALES WITH THE FMR1 PREMUTATIONP30HD024064 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI ZOGHBI, HUDA Y · 1988 to 2013
$29.4M
NRI Build-out: Advancing Translational Brain ResearchC06RR029965 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI ZOGHBI, HUDA Y · 2010 to 2010
$14.9M
Steps towards a paternal gene activation therapy for Angelman syndromeU54HD083092 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN, NELSON, DAVID LOREN · 2014 to 2019
$7.8M
SYNAPTIC ORIGINS OF CEREBELLAR DISEASER01NS089664 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI SILLITOE, ROY VINCENT · 2014 to 2018
$1.7M
NCRR NIH HHS C06 RR029965NCRR NIH HHS C06RR029965NICHD NIH HHS 5P30HD024064NICHD NIH HHS P30 HD024064NICHD NIH HHS U54 HD083092NINDS NIH HHS R01 NS089664
6 · The paper itself

Abstract

Cerebellar circuits are patterned into an array of topographic parasagittal domains called zones. The proper connectivity of zones is critical for motor coordination and motor learning, and in several neurological diseases cerebellar circuits degenerate in zonal patterns. Despite recent advances in understanding zone function, we still have a limited understanding of how zones are formed. Here, we focused our attention on Purkinje cells to gain a better understanding of their specific role in establishing zonal circuits. We used conditional mouse genetics to test the hypothesis that Purkinje cell neurotransmission is essential for refining prefunctional developmental zones into sharp functional zones. Our results show that inhibitory synaptic transmission in Purkinje cells is necessary for the precise patterning of Purkinje cell zones and the topographic targeting of mossy fiber afferents. As expected, blocking Purkinje cell neurotransmission caused ataxia. Using in vivo electrophysiology, we demonstrate that loss of Purkinje cell communication altered the firing rate and pattern of their target cerebellar nuclear neurons. Analysis of Purkinje cell complex spike firing revealed that feedback in the cerebellar nuclei to inferior olive to Purkinje cell loop is obstructed. Loss of Purkinje neurotransmission also caused ectopic zonal expression of tyrosine hydroxylase, which is only expressed in adult Purkinje cells when calcium is dysregulated and if excitability is altered. Our results suggest that Purkinje cell inhibitory neurotransmission establishes the functional circuitry of the cerebellum by patterning the molecular zones, fine-tuning afferent circuitry, and shaping neuronal activity.

Indexed as

CerebellumAge FactorsAnimalsAnimals, NewbornBody WeightEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalMaleMiceMice, TransgenicMovement DisordersMutationNerve Tissue ProteinsNeural InhibitionOrgan SizeNerve Tissue ProteinsPurkinje cell protein L7Vesicular Inhibitory Amino Acid Transport ProteinsViaat protein, mouseataxiacircuitryconnectivitygene expressioninhibitionphysiology

Identifiers

PMID24920627
PMCPMC4051975
OpenAlexW2000339987

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.