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Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine–induced temporal lobe epilepsy model

Overview of attention for article published in Frontiers in Cellular Neuroscience, January 2013
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Title
Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine–induced temporal lobe epilepsy model
Published in
Frontiers in Cellular Neuroscience, January 2013
DOI 10.3389/fncel.2013.00104
Pubmed ID
Authors

Yuki Nagao, Yuya Harada, Takahiro Mukai, Saki Shimizu, Aoi Okuda, Megumi Fujimoto, Asuka Ono, Yoshihisa Sakagami, Yukihiro Ohno

Abstract

The inwardly rectifying potassium (Kir) channel Kir4.1 in brain astrocytes mediates spatial K(+) buffering and regulates neural activities. Recent studies have shown that loss-of-function mutations in the human gene KCNJ10 encoding Kir4.1 cause epileptic seizures, suggesting a close relationship between the Kir4.1 channel function and epileptogenesis. Here, we performed expressional analysis of Kir4.1 in a pilocarpine-induced rat model of temporal lobe epilepsy (TLE) to explore the role of Kir4.1 channels in modifying TLE epileptogenesis. Treatment of rats with pilocarpine (350 mg/kg, i.p.) induced acute status epilepticus, which subsequently caused spontaneous seizures 7-8 weeks after the pilocarpine treatment. Western blot analysis revealed that TLE rats (interictal condition) showed significantly higher levels of Kir4.1 than the control animals in the cerebral cortex, striatum, and hypothalamus. However, the expression of other Kir subunits, Kir5.1 and Kir2.1, remained unaltered. Immunohistochemical analysis illustrated that Kir4.1-immunoreactivity-positive astrocytes in the pilocarpine-induced TLE model were markedly increased in most of the brain regions examined, concomitant with an increase in the number of glial fibrillary acidic protein (GFAP)-positive astrocytes. In addition, Kir4.1 expression ratios relative to the number of astrocytes (Kir4.1-positive cells/GFAP-positive cells) were region-specifically elevated in the amygdala (i.e., medial and cortical amygdaloid nuclei) and sensory cortex. The present study demonstrated for the first time that the expression of astrocytic Kir4.1 channels was elevated in a pilocarpine-induced TLE model, especially in the amygdala, suggesting that astrocytic Kir4.1 channels play a role in modifying TLE epileptogenesis, possibly by acting as an inhibitory compensatory mechanism.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 73 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 2 3%
Mexico 1 1%
Unknown 70 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 19 26%
Researcher 13 18%
Student > Master 9 12%
Student > Bachelor 6 8%
Professor > Associate Professor 5 7%
Other 11 15%
Unknown 10 14%
Readers by discipline Count As %
Agricultural and Biological Sciences 20 27%
Neuroscience 14 19%
Biochemistry, Genetics and Molecular Biology 8 11%
Medicine and Dentistry 8 11%
Pharmacology, Toxicology and Pharmaceutical Science 6 8%
Other 6 8%
Unknown 11 15%
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 05 July 2013.
All research outputs
#20,195,877
of 22,713,403 outputs
Outputs from Frontiers in Cellular Neuroscience
#3,547
of 4,211 outputs
Outputs of similar age
#248,765
of 280,747 outputs
Outputs of similar age from Frontiers in Cellular Neuroscience
#156
of 203 outputs
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So far Altmetric has tracked 4,211 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.2. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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