↓ Skip to main content

RCAN1 Knockdown Reverts Defects in the Number of Calcium-Induced Exocytotic Events in a Cellular Model of Down Syndrome

Overview of attention for article published in Frontiers in Cellular Neuroscience, July 2018
Altmetric Badge

Mentioned by

twitter
2 X users

Readers on

mendeley
12 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
RCAN1 Knockdown Reverts Defects in the Number of Calcium-Induced Exocytotic Events in a Cellular Model of Down Syndrome
Published in
Frontiers in Cellular Neuroscience, July 2018
DOI 10.3389/fncel.2018.00189
Pubmed ID
Authors

Jacqueline Vásquez-Navarrete, Agustín D. Martínez, Stéphane Ory, Ximena Baéz-Matus, Arlek M. González-Jamett, Sebastián Brauchi, Pablo Caviedes, Ana M. Cárdenas

Abstract

In humans, Down Syndrome (DS) is a condition caused by partial or full trisomy of chromosome 21. Genes present in the DS critical region can result in excess gene dosage, which at least partially can account for DS phenotype. Although regulator of calcineurin 1 (RCAN1) belongs to this region and its ectopic overexpression in neurons impairs transmitter release, synaptic plasticity, learning and memory, the relative contribution of RCAN1 in a context of DS has yet to be clarified. In the present work, we utilized an in vitro model of DS, the CTb neuronal cell line derived from the brain cortex of a trisomy 16 (Ts16) fetal mouse, which reportedly exhibits acetylcholine release impairments compared to CNh cells (a neuronal cell line established from a normal littermate). We analyzed single exocytotic events by using total internal reflection fluorescence microscopy (TIRFM) and the vesicular acetylcholine transporter fused to the pH-sensitive green fluorescent protein (VAChT-pHluorin) as a reporter. Our analyses showed that, compared with control CNh cells, the trisomic CTb cells overexpress RCAN1, and they display a reduced number of Ca2+-induced exocytotic events. Remarkably, RCAN1 knockdown increases the extent of exocytosis at levels comparable to those of CNh cells. These results support a critical contribution of RCAN1 to the exocytosis process in the trisomic condition.

X Demographics

X Demographics

The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 12 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 12 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 4 33%
Student > Ph. D. Student 2 17%
Student > Doctoral Student 1 8%
Other 1 8%
Professor > Associate Professor 1 8%
Other 0 0%
Unknown 3 25%
Readers by discipline Count As %
Agricultural and Biological Sciences 3 25%
Neuroscience 2 17%
Biochemistry, Genetics and Molecular Biology 1 8%
Social Sciences 1 8%
Chemistry 1 8%
Other 0 0%
Unknown 4 33%
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 24 July 2018.
All research outputs
#18,643,992
of 23,096,849 outputs
Outputs from Frontiers in Cellular Neuroscience
#3,284
of 4,279 outputs
Outputs of similar age
#252,936
of 327,716 outputs
Outputs of similar age from Frontiers in Cellular Neuroscience
#88
of 115 outputs
Altmetric has tracked 23,096,849 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 4,279 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.3. This one is in the 15th percentile – i.e., 15% 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 327,716 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 12th percentile – i.e., 12% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 115 others from the same source and published within six weeks on either side of this one. This one is in the 13th percentile – i.e., 13% of its contemporaries scored the same or lower than it.