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Eag1 potassium channel immunohistochemistry in the CNS of adult rat and selected regions of human brain
Eag1 (K V10.1) is the founding member of an evolutionarily conserved superfamily of voltage-gated K + channels. In rats and humans Eag1 is preferentially expressed in adult brain but its regional distribution has only been studied at mRNA level and only in the rat at high resolution. The main aim of...
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Published in: | Neuroscience 2008-08, Vol.155 (3), p.833-844 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Eag1 (K
V10.1) is the founding member of an evolutionarily conserved superfamily of voltage-gated K
+ channels. In rats and humans
Eag1 is preferentially expressed in adult brain but its regional distribution has only been studied at mRNA level and only in the rat at high resolution. The main aim of the present study is to describe the distribution of
Eag1 protein in adult rat brain in comparison to selected regions of the human adult brain. The distribution of
Eag1 protein was assessed using alkaline-phosphatase based immunohistochemistry.
Eag1 immunoreactivity was widespread, although selective, throughout rat brain, especially noticeable in the perinuclear space of cells and proximal regions of the extensions, both in rat and human brain. To relate the results to the relative abundance of
Eag1 transcripts in different regions of rat brain a reverse-transcription coupled to quantitative polymerase chain reaction (real time PCR) was performed. This real time PCR analysis showed high
Eag1 expression in the olfactory bulb, cerebral cortex, hippocampus, hypothalamus, and cerebellum. The results indicate that
Eag1 protein expression greatly overlaps with mRNA distribution in rats and humans. The physiological relevance of potassium channels in the different regions expressing
Eag1 protein is discussed. |
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ISSN: | 0306-4522 1873-7544 |
DOI: | 10.1016/j.neuroscience.2008.05.019 |