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Bilateral neuroinflammatory processes in visual pathways induced by unilateral ocular hypertension in the rat

Overview of attention for article published in Journal of Neuroinflammation, February 2016
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Title
Bilateral neuroinflammatory processes in visual pathways induced by unilateral ocular hypertension in the rat
Published in
Journal of Neuroinflammation, February 2016
DOI 10.1186/s12974-016-0509-7
Pubmed ID
Authors

Anaïs Sapienza, Anne-Laure Raveu, Elodie Reboussin, Christophe Roubeix, Céline Boucher, Julie Dégardin, David Godefroy, William Rostène, Annabelle Reaux-Le Goazigo, Christophe Baudouin, Stéphane Melik Parsadaniantz

Abstract

Glaucoma is one of the leading causes of irreversible blindness in the world. The major risk factor is elevated intraocular pressure (IOP) leading to progressive retinal ganglion cell (RGC) death from the optic nerve (ON) to visual pathways in the brain. Glaucoma has been reported to share mechanisms with neurodegenerative disorders. We therefore hypothesize that neuroinflammatory mechanisms in central visual pathways may contribute to the spread of glaucoma disease. The aim of the present study was to analyze the neuroinflammation processes that occur from the pathological retina to the superior colliculi (SCs) in a rat model of unilateral ocular hypertension induced by episcleral vein cauterization (EVC). Six weeks after unilateral (right eye) EVC in male Long-Evans rats, we evaluated both the neurodegenerative process and the neuroinflammatory state in visual pathway tissues. RGCs immunolabeled (Brn3a(+)) in ipsilateral whole flat-mounted retina demonstrated peripheral RGC loss associated with tissue macrophage/microglia activation (CD68(+)). Gene expression analysis of hypertensive and normotensive retinas revealed a significant increase of pro-inflammatory genes such as CCL2, IL-1β, and Nox2 mRNA expression compared to naïve eyes. Importantly, we found an upregulation of pro-inflammatory markers such as IL-1β and TNFα and astrocyte and tissue macrophage/microglia activation in hypertensive and normotensive RGC projection sites in the SCs compared to a naïve SC. To understand how neuroinflammation in the hypertensive retina is sufficient to damage both right and left SCs and the normotensive retina, we used an inflammatory model consisting in an unilateral stereotaxic injection of TNFα (25 ng/μl) in the right SC of naïve rats. Two weeks after TNFα injection, using an optomotor test, we observed that rats had visual deficiency in both eyes. Furthermore, both SCs showed an upregulation of genes and proteins for astrocytes, microglia, and pro-inflammatory cytokines, notably IL-1β. In addition, both retinas exhibited a significant increase of inflammatory markers compared to a naïve retina. All these data evidence the complex role played by the SCs in the propagation of neuroinflammatory events induced by unilateral ocular hypertension and provide a new insight into the spread of neurodegenerative diseases such as glaucoma.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 70 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 1%
Unknown 69 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 16 23%
Student > Master 10 14%
Researcher 7 10%
Student > Doctoral Student 5 7%
Student > Bachelor 4 6%
Other 12 17%
Unknown 16 23%
Readers by discipline Count As %
Neuroscience 22 31%
Medicine and Dentistry 10 14%
Biochemistry, Genetics and Molecular Biology 5 7%
Agricultural and Biological Sciences 5 7%
Psychology 3 4%
Other 5 7%
Unknown 20 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 February 2016.
All research outputs
#17,285,036
of 25,371,288 outputs
Outputs from Journal of Neuroinflammation
#2,022
of 2,951 outputs
Outputs of similar age
#188,811
of 312,181 outputs
Outputs of similar age from Journal of Neuroinflammation
#33
of 54 outputs
Altmetric has tracked 25,371,288 research outputs across all sources so far. This one is in the 21st percentile – i.e., 21% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,951 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.7. This one is in the 23rd percentile – i.e., 23% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 312,181 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 31st percentile – i.e., 31% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 54 others from the same source and published within six weeks on either side of this one. This one is in the 29th percentile – i.e., 29% of its contemporaries scored the same or lower than it.