RGD Reference Report - Changes in the astrocytic aquaporin-4 and inwardly rectifying potassium channel expression in the brain of the amyotrophic lateral sclerosis SOD1(G93A) rat model. - Rat Genome Database

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Changes in the astrocytic aquaporin-4 and inwardly rectifying potassium channel expression in the brain of the amyotrophic lateral sclerosis SOD1(G93A) rat model.

Authors: Bataveljic, D  Nikolic, L  Milosevic, M  Todorovic, N  Andjus, PR 
Citation: Bataveljic D, etal., Glia. 2012 Dec;60(12):1991-2003. doi: 10.1002/glia.22414. Epub 2012 Sep 14.
RGD ID: 8662893
Pubmed: PMID:22987392   (View Abstract at PubMed)
DOI: DOI:10.1002/glia.22414   (Journal Full-text)

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting upper and lower motor neurons. Dysfunction and death of motor neurons are closely related to the modified astrocytic environment. Astrocytic endfeet, lining the blood-brain barrier (BBB), are enriched in two proteins, aquaporin-4 (AQP4) and inwardly rectifying potassium channel (Kir) 4.1. Both channels are important for the maintainance of a functional BBB astrocytic lining. In this study, expression levels of AQP4 and Kir4.1 were for the first time examined in the brainstem and cortex, along with the functional properties of Kir channels in cultured cortical astrocytes of the SOD1(G93A) rat model of ALS. Western blot analysis showed increased expression of AQP4 and decreased expression of Kir4.1 in the brainstem and cortex of the ALS rat. In addition, higher immunoreactivity of AQP4 and reduced immunolabeling of Kir4.1 in facial and trigeminal nuclei as well as in the motor cortex were also observed. Particularly, the observed changes in the expression of both channels were retained in cultured astrocytes. Furthermore, whole-cell patch-clamp recordings from cultured ALS cortical astrocytes showed a significantly lower Kir current density. Importantly, the potassium uptake current in ALS astrocytes was significantly reduced at all extracellular potassium concentrations. Consequently, the Kir-specific Cs(+)- and Ba(2+)-sensitive currents were also decreased. The changes in the studied channels, notably at the upper CNS level, could underline the hampered ability of astrocytes to maintain water and potassium homeostasis, thus affecting the BBB, disturbing the neuronal microenvironment, and causing motoneuronal dysfunction and death.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
amyotrophic lateral sclerosis  ISOAqp4 (Rattus norvegicus)8662893; 8662893protein:increased expression:brainstemRGD 
amyotrophic lateral sclerosis  IEP 8662893protein:increased expression:brainstemRGD 
amyotrophic lateral sclerosis  ISOKcnj10 (Rattus norvegicus)8662893; 8662893protein:decreased expression:brainstemRGD 
amyotrophic lateral sclerosis  IEP 8662893protein:decreased expression:brainstemRGD 

Objects Annotated

Genes (Rattus norvegicus)
Aqp4  (aquaporin 4)
Kcnj10  (potassium inwardly-rectifying channel, subfamily J, member 10)

Genes (Mus musculus)
Aqp4  (aquaporin 4)
Kcnj10  (potassium inwardly-rectifying channel, subfamily J, member 10)

Genes (Homo sapiens)
AQP4  (aquaporin 4)
KCNJ10  (potassium inwardly rectifying channel subfamily J member 10)


Additional Information