Evidence map›Paper›PMID 26441550›Full record

ReviewFrontiers in neuroanatomy2015

Morphological changes of glutamatergic synapses in animal models of Parkinson's disease.

Rosa M Villalba, Abraham Mathai, Yoland Smith

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroanatomy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.1field-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

35 citing papers in PubMed, 67 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Rosa M VillalbaYerkes National Primate Research Center, Emory University Atlanta, GA, USA ; UDALL Center of Excellence for Parkinson's Disease, Emory University Atlanta, GA, USA.
Abraham MathaiYerkes National Primate Research Center, Emory University Atlanta, GA, USA ; UDALL Center of Excellence for Parkinson's Disease, Emory University Atlanta, GA, USA.
Yoland SmithYerkes National Primate Research Center, Emory University Atlanta, GA, USA ; UDALL Center of Excellence for Parkinson's Disease, Emory University Atlanta, GA, USA ; Department of Neurology, Emory University Atlanta, GA, USA.
Emory University · US

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
Udall Parkinson's Disease Center at Emory University: Circuitry to TherapyP50NS071669 · NINDS · EMORY UNIVERSITY · PI WICHMANN, THOMAS · 2010 to 2015
$6.8M
The Thalamostriatal System in PrimateR01NS037948 · NINDS · EMORY UNIVERSITY · PI SMITH, YOLAND · 1998 to 2013
$3.7M
Thalamic interactions with the striatumR01NS083386 · NINDS · EMORY UNIVERSITY · PI WICHMANN, THOMAS · 2013 to 2017
$2.1M
NIH HHS P51 OD011132NINDS NIH HHS P50 NS071669NINDS NIH HHS R01 NS037948NINDS NIH HHS R01 NS083386
6 · The paper itself

Abstract

The striatum and the subthalamic nucleus (STN) are the main entry doors for extrinsic inputs to reach the basal ganglia (BG) circuitry. The cerebral cortex, thalamus and brainstem are the key sources of glutamatergic inputs to these nuclei. There is anatomical, functional and neurochemical evidence that glutamatergic neurotransmission is altered in the striatum and STN of animal models of Parkinson's disease (PD) and that these changes may contribute to aberrant network neuronal activity in the BG-thalamocortical circuitry. Postmortem studies of animal models and PD patients have revealed significant pathology of glutamatergic synapses, dendritic spines and microcircuits in the striatum of parkinsonians. More recent findings have also demonstrated a significant breakdown of the glutamatergic corticosubthalamic system in parkinsonian monkeys. In this review, we will discuss evidence for synaptic glutamatergic dysfunction and pathology of cortical and thalamic inputs to the striatum and STN in models of PD. The potential functional implication of these alterations on synaptic integration, processing and transmission of extrinsic information through the BG circuits will be considered. Finally, the significance of these pathological changes in the pathophysiology of motor and non-motor symptoms in PD will be examined.

Indexed as

astrocytes plasticityglutamatergic synapsesParkinson’s diseasestriatumsubthalamic nucleussynaptic plasticityvGluT

Identifiers

PMID26441550
PMCPMC4585113
OpenAlexW2109554447

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.