Expressional analysis of inwardly rectifying Kir4.1 channels in Noda epileptic rat (NER)

Abstract The inwardly rectifying potassium channel subunit Kir4.1 is expressed in brain astrocytes and involved in spatial K+ buffering, regulating neural activity. To explore the pathophysiological alterations of Kir4.1 channels in epileptic disorders, we analyzed interictal expressional levels of...

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Bibliographic Details
Published in:Brain research 2013-06, Vol.1517, p.141-149
Main Authors: Harada, Yuya, Nagao, Yuki, Shimizu, Saki, Serikawa, Tadao, Terada, Ryo, Fujimoto, Megumi, Okuda, Aoi, Mukai, Takahiro, Sasa, Masashi, Kurachi, Yoshihisa, Ohno, Yukihiro
Format: Article
Language:English
Subjects:
Amygdala
Amygdala - pathology
Animals
Astrocyte
Biological and medical sciences
Disease Models, Animal
Epilepsy, Tonic-Clonic - genetics
Epilepsy, Tonic-Clonic - metabolism
Epilepsy, Tonic-Clonic - pathology
Gene Expression Regulation - genetics
Gene Expression Regulation - physiology
Generalized tonic-clonic (GTC) seizure
Glial Fibrillary Acidic Protein - metabolism
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Kir4.1 channel
Male
Medical sciences
Nervous system (semeiology, syndromes)
Neuroglia - metabolism
Neurology
Neurons - metabolism
Noda epileptic rat (NER)
Oncogene Proteins v-fos - metabolism
Phosphopyruvate Hydratase - metabolism
Potassium Channels, Inwardly Rectifying - genetics
Potassium Channels, Inwardly Rectifying - metabolism
Rats
Rats, Inbred WKY
Rats, Mutant Strains
Spatial potassium buffering
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Summary:Abstract The inwardly rectifying potassium channel subunit Kir4.1 is expressed in brain astrocytes and involved in spatial K+ buffering, regulating neural activity. To explore the pathophysiological alterations of Kir4.1 channels in epileptic disorders, we analyzed interictal expressional levels of Kir4.1 in the Noda epileptic rat (NER), a hereditary animal model for generalized tonic-clonic (GTC) seizures. Western blot analysis showed that Kir4.1 expression in NERs was significantly reduced in the occipito-temporal cortical region and thalamus. However, the expression of Kir5.1, another Kir subunit mediating spatial K+ buffering, remained unaltered in any brain regions examined. Immunohistochemical analysis revealed that Kir4.1 was primarily expressed in glial fibrillary acidic protein (GFAP)-positive astrocytes (somata) and foot processes clustered around neurons proved with anti-neuronal nuclear antigen (NeuN) antibody. In NERs, Kir4.1 expression in astrocytic processes was region-selectively diminished in the amygdaloid nuclei (i.e., medial amygdaloid nucleus and basomedial amygdaloid nucleus) while Kir4.1 expression in astrocytic somata was unchanged. Furthermore, the amygdala regions with reduced Kir4.1 expression showed a marked elevation of Fos protein expression following GTC seizures. The present results suggest that reduced activity of astrocytic Kir4.1 channels in the amygdala is involved in limbic hyperexcitability in NERs.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2013.04.009