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Cerebellar Kainate Receptor-Mediated Facilitation of Glutamate Release Requires Ca2+-Calmodulin and PKA

Overview of attention for article published in Frontiers in Molecular Neuroscience, June 2018
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Title
Cerebellar Kainate Receptor-Mediated Facilitation of Glutamate Release Requires Ca2+-Calmodulin and PKA
Published in
Frontiers in Molecular Neuroscience, June 2018
DOI 10.3389/fnmol.2018.00195
Pubmed ID
Authors

Rafael Falcón-Moya, Pilar Losada-Ruiz, Talvinder S. Sihra, Antonio Rodríguez-Moreno

Abstract

We elucidated the mechanisms underlying the kainate receptor (KAR)-mediated facilitatory modulation of synaptic transmission in the cerebellum. In cerebellar slices, KA (3 μM) increased the amplitude of evoked excitatory postsynaptic currents (eEPSCs) at synapses between axon terminals of parallel fibers (PF) and Purkinje neurons. KA-mediated facilitation was antagonized by NBQX under condition where AMPA receptors were previously antagonized. Inhibition of protein kinase A (PKA) suppressed the effect of KA on glutamate release, which was also obviated by the prior stimulation of adenylyl cyclase (AC). KAR-mediated facilitation of synaptic transmission was prevented by blocking Ca2+ permeant KARs using philanthotoxin. Furthermore, depletion of intracellular Ca2+ stores by thapsigargin, or inhibition of Ca2+-induced Ca2+-release by ryanodine, abrogated the synaptic facilitation by KA. Thus, the KA-mediated modulation was conditional on extracellular Ca2+ entry through Ca2+-permeable KARs, as well as and mobilization of Ca2+ from intracellular stores. Finally, KAR-mediated facilitation was sensitive to calmodulin inhibitors, W-7 and calmidazolium, indicating that the increased cytosolic [Ca2+] sustaining KAR-mediated facilitation of synaptic transmission operates through a downstream Ca2+/calmodulin coupling. We conclude that, at cerebellar parallel fiber-Purkinje cell synapses, presynaptic KARs mediate glutamate release facilitation, and thereby enhance synaptic transmission through Ca2+-calmodulin dependent activation of adenylyl cyclase/cAMP/protein kinase A signaling.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 25 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 25 100%

Demographic breakdown

Readers by professional status Count As %
Professor 3 12%
Student > Ph. D. Student 3 12%
Student > Doctoral Student 2 8%
Student > Bachelor 2 8%
Librarian 2 8%
Other 4 16%
Unknown 9 36%
Readers by discipline Count As %
Neuroscience 8 32%
Agricultural and Biological Sciences 2 8%
Engineering 2 8%
Psychology 1 4%
Environmental Science 1 4%
Other 2 8%
Unknown 9 36%
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 08 April 2019.
All research outputs
#17,980,413
of 23,090,520 outputs
Outputs from Frontiers in Molecular Neuroscience
#2,087
of 2,929 outputs
Outputs of similar age
#238,173
of 329,353 outputs
Outputs of similar age from Frontiers in Molecular Neuroscience
#78
of 116 outputs
Altmetric has tracked 23,090,520 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,929 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one is in the 21st percentile – i.e., 21% of its peers scored the same or lower than it.
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We're also able to compare this research output to 116 others from the same source and published within six weeks on either side of this one. This one is in the 21st percentile – i.e., 21% of its contemporaries scored the same or lower than it.