Evidence map›Paper›PMID 28377699›Full record

ArticleFrontiers in neuroanatomy2017

Computational Model of Recurrent Subthalamo-Pallidal Circuit for Generation of Parkinsonian Oscillations.

Osamu Shouno, Yoshihisa Tachibana, Atsushi Nambu, Kenji Doya

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroanatomy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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  17. Multistable properties of human subthalamic nucleus neurons in Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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 3 institutions in 1 country.

Osamu ShounoOkinawa Institute of Science and Technology Graduate UniversityOkinawa, Japan; Honda Research Institute Japan Co., Ltd.Saitama, Japan.
Yoshihisa TachibanaDivision of System Neurophysiology, Department of Physiological Sciences, National Institute for Physiological Sciences, Graduate University for Advanced Studies Aichi, Japan.
Atsushi NambuDivision of System Neurophysiology, Department of Physiological Sciences, National Institute for Physiological Sciences, Graduate University for Advanced Studies Aichi, Japan.
Kenji DoyaOkinawa Institute of Science and Technology Graduate University Okinawa, Japan.
National Institute for Physiological Sciences · JPHonda (Japan) · JPOkinawa Institute of Science and Technology Graduate University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease is a movement disorder caused by dopamine depletion in the basal ganglia. Abnormally synchronized neuronal oscillations between 8 and 15 Hz in the basal ganglia are implicated in motor symptoms of Parkinson's disease. However, how these abnormal oscillations are generated and maintained in the dopamine-depleted state is unknown. Based on neural recordings in a primate model of Parkinson's disease and other experimental and computational evidence, we hypothesized that the recurrent circuit between the subthalamic nucleus (STN) and the external segment of the globus pallidus (GPe) generates and maintains parkinsonian oscillations, and that the cortical excitatory input to the STN amplifies them. To investigate this hypothesis through computer simulations, we developed a spiking neuron model of the STN-GPe circuit by incorporating electrophysiological properties of neurons and synapses. A systematic parameter search by computer simulation identified regions in the space of the intrinsic excitability of GPe neurons and synaptic strength from the GPe to the STN that reproduce normal and parkinsonian states. In the parkinsonian state, reduced firing of GPe neurons and increased GPe-STN inhibition trigger burst activities of STN neurons with strong post-inhibitory rebound excitation, which is usually subject to short-term depression. STN neuronal bursts are shaped into the 8-15 Hz, synchronous oscillations via recurrent interactions of STN and GPe neurons. Furthermore, we show that cortical excitatory input to the STN can amplify or suppress pathological STN oscillations depending on their phase and strength, predicting conditions of cortical inputs to the STN for suppressing oscillations.

Indexed as

basal gangliabeta oscillationglobus pallidusparkinsonian oscillationrebound excitatonshort-term plasticitysubthalamic nucleus

Identifiers

PMID28377699
PMCPMC5359256
OpenAlexW2598636654

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.