Evidence map›Paper›PMID 24899724›Full record

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

The substantia nigra conveys target-dependent excitatory and inhibitory outputs from the basal ganglia to the thalamus.

Miklos Antal, Brandon M Beneduce, Wade G Regehr

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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-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

31 citing papers in PubMed, 63 citations in OpenAlex.

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  12. Substantia Nigra Pars Reticulata Projections to the Pedunculopontine Nucleus Modulate Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2023
    Article
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  17. The relationship between attention and static balance disturbance in patients with Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Article
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  20. 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

3 authors at 1 institution in 1 country.

Miklos AntalDepartment of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115.
Brandon M BeneduceDepartment of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115.
Wade G RegehrDepartment of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115 wade_regehr@hms.harvard.edu.
Harvard University · US

Funding

Super-Resolution ImagingP30NS072030 · NINDS · HARVARD MEDICAL SCHOOL · PI REGEHR, WADE G · 2011 to 2020
$5.8M
Short-Term Synaptic Plasticity in the CNSR01NS032405 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI REGEHR, WADE G · 1995 to 2016
$4.8M
NINDS NIH HHS NS072030NINDS NIH HHS P30 NS072030NINDS NIH HHS R01 NS032405NINDS NIH HHS R01NS032405
6 · The paper itself

Abstract

The basal ganglia (BG), which influence cortical activity via the thalamus, play a major role in motor activity, learning and memory, sensory processing, and many aspects of behavior. The substantia nigra (SN) consists of GABAergic neurons of the pars reticulata that inhibit thalamic neurons and provide the primary output of the BG, and dopaminergic neurons of the pars compacta that modulate thalamic excitability. Little is known about the functional properties of the SN→thalamus synapses, and anatomical characterization has been controversial. Here we use a combination of anatomical, electrophysiological, genetic, and optogenetic approaches to re-examine these synaptic connections in mice. We find that neurons in the SN inhibit neurons in the ventroposterolateral nucleus of the thalamus via GABAergic synapses, excite neurons in the thalamic nucleus reticularis, and both excite and inhibit neurons within the posterior nucleus group. Glutamatergic SN neurons express the vesicular glutamate receptor transporter vGluT2 and receive inhibitory synapses from striatal neurons, and many also express tyrosine hydroxylase, a marker of dopaminergic neurons. Thus, in addition to providing inhibitory outputs, which is consistent with the canonical circuit, the SN provides glutamatergic outputs that differentially target thalamic nuclei. This suggests that an increase in the activity of glutamatergic neurons in the SN allows the BG to directly excite neurons in specific thalamic nuclei. Elucidating an excitatory connection between the BG and the thalamus provides new insights into how the BG regulate thalamic activity, and has important implications for understanding BG function in health and disease.

Indexed as

Action PotentialsAnimalsBasal GangliaChannelrhodopsinsDependovirusGlutamate DecarboxylaseIn Vitro TechniquesMiceMice, Inbred C57BLMice, TransgenicNeural InhibitionNeural PathwaysNeurotransmitter AgentsPhotic StimulationSubstantia NigraThalamusChannelrhodopsinsGlutamate Decarboxylaseglutamate decarboxylase 1Neurotransmitter AgentsSlc17a6 protein, mouseVesicular Glutamate Transport Protein 2circuitrysubstantia nigravGluT2

Identifiers

PMID24899724
PMCPMC4044258
OpenAlexW1967305873

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.