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Deletion of aquaporin-4 increases extracellular K(+) concentration during synaptic stimulation in mouse hippocampus.

Haj-Yasein NN, Bugge CE, Jensen V, Østby I, Ottersen OP, Hvalby Ø, Nagelhus EA - Brain Struct Funct (2014)

Bottom Line: We show that Aqp4 deletion has a layer-specific effect on [K(+)]o that precisely mirrors the known effect on extracellular volume dynamics.In stratum pyramidale and corpus callosum, neither peak [K(+)]o nor post-stimulus [K(+)]o recovery was affected by Aqp4 deletion.Our data suggest that AQP4 modulates [K(+)]o during synaptic stimulation through its effect on extracellular space volume.

View Article: PubMed Central - PubMed

Affiliation: Letten Centre, Institute of Basic Medical Sciences, University of Oslo, 0317, Oslo, Norway.

ABSTRACT
The coupling between the water channel aquaporin-4 (AQP4) and K(+) transport has attracted much interest. In this study, we assessed the effect of Aqp4 deletion on activity-induced [K(+)]o changes in acute slices from hippocampus and corpus callosum of adult mice. We show that Aqp4 deletion has a layer-specific effect on [K(+)]o that precisely mirrors the known effect on extracellular volume dynamics. In CA1, the peak [K(+)]o in stratum radiatum during 20 Hz stimulation of Schaffer collateral/commissural fibers was significantly higher in Aqp4 (-/-) mice than in wild types, whereas no differences were observed throughout the [K(+)]o recovery phase. In stratum pyramidale and corpus callosum, neither peak [K(+)]o nor post-stimulus [K(+)]o recovery was affected by Aqp4 deletion. Our data suggest that AQP4 modulates [K(+)]o during synaptic stimulation through its effect on extracellular space volume.

No MeSH data available.


Related in: MedlinePlus

Distribution of AQP4 and Kir4.1 immunofluorescence in acute slices from hippocampus and corpus callosum. AQP4 labeling in stratum radiatum (rad) and stratum pyramidale (pyr) of the hippocampal CA1 region (a) and in coronal corpus callosum (c) from wild type mice. In both regions, a reticular staining pattern was observed, compatible with labeling of fine astrocytic processes. The intense signal around blood vessels corresponds to astrocytic endfeet (arrowheads). The selectivity of antibodies was confirmed by absence of AQP4 labeling in slices from Aqp4−/− mice (e, g). Kir4.1 immunofluorescence likewise outlined delicate processes resembling those of astrocytes (b, d), with less prominent perivascular signal (arrowhead) than observed with antibodies against AQP4. Kir4.1 immunoreactivity in hippocampus (f) and corpus (h) callosum of Aqp4−/− mice was similar to that of wild types. Scale bar 100 µm
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Fig1: Distribution of AQP4 and Kir4.1 immunofluorescence in acute slices from hippocampus and corpus callosum. AQP4 labeling in stratum radiatum (rad) and stratum pyramidale (pyr) of the hippocampal CA1 region (a) and in coronal corpus callosum (c) from wild type mice. In both regions, a reticular staining pattern was observed, compatible with labeling of fine astrocytic processes. The intense signal around blood vessels corresponds to astrocytic endfeet (arrowheads). The selectivity of antibodies was confirmed by absence of AQP4 labeling in slices from Aqp4−/− mice (e, g). Kir4.1 immunofluorescence likewise outlined delicate processes resembling those of astrocytes (b, d), with less prominent perivascular signal (arrowhead) than observed with antibodies against AQP4. Kir4.1 immunoreactivity in hippocampus (f) and corpus (h) callosum of Aqp4−/− mice was similar to that of wild types. Scale bar 100 µm

Mentions: AQP4 immunofluorescence of immersion fixed tissue slices revealed a reticular labeling pattern compatible with staining of astrocytic processes in both hippocampus (Fig. 1a) and corpus callosum (Fig. 1c). Intense labeling was observed around blood vessels. Absence of AQP4 labeling in Aqp4−/− mice confirmed the selectivity of antibodies (Fig. 1e, g). Kir4.1 immunoreactivity in wild type animals resembled that of AQP4, but the signal was weaker around vessels (Fig. 1b, d). Importantly, the pattern of Kir4.1 immunoreactivity in hippocampus and corpus callosum was unaffected by Aqp4 deletion (Fig. 1f, h). The distribution of AQP4 and Kir4.1 labeling of immersion fixed slices was similar to that of perfusion fixed tissue (cf. Haj-Yasein et al. 2011).Fig. 1


Deletion of aquaporin-4 increases extracellular K(+) concentration during synaptic stimulation in mouse hippocampus.

Haj-Yasein NN, Bugge CE, Jensen V, Østby I, Ottersen OP, Hvalby Ø, Nagelhus EA - Brain Struct Funct (2014)

Distribution of AQP4 and Kir4.1 immunofluorescence in acute slices from hippocampus and corpus callosum. AQP4 labeling in stratum radiatum (rad) and stratum pyramidale (pyr) of the hippocampal CA1 region (a) and in coronal corpus callosum (c) from wild type mice. In both regions, a reticular staining pattern was observed, compatible with labeling of fine astrocytic processes. The intense signal around blood vessels corresponds to astrocytic endfeet (arrowheads). The selectivity of antibodies was confirmed by absence of AQP4 labeling in slices from Aqp4−/− mice (e, g). Kir4.1 immunofluorescence likewise outlined delicate processes resembling those of astrocytes (b, d), with less prominent perivascular signal (arrowhead) than observed with antibodies against AQP4. Kir4.1 immunoreactivity in hippocampus (f) and corpus (h) callosum of Aqp4−/− mice was similar to that of wild types. Scale bar 100 µm
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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Fig1: Distribution of AQP4 and Kir4.1 immunofluorescence in acute slices from hippocampus and corpus callosum. AQP4 labeling in stratum radiatum (rad) and stratum pyramidale (pyr) of the hippocampal CA1 region (a) and in coronal corpus callosum (c) from wild type mice. In both regions, a reticular staining pattern was observed, compatible with labeling of fine astrocytic processes. The intense signal around blood vessels corresponds to astrocytic endfeet (arrowheads). The selectivity of antibodies was confirmed by absence of AQP4 labeling in slices from Aqp4−/− mice (e, g). Kir4.1 immunofluorescence likewise outlined delicate processes resembling those of astrocytes (b, d), with less prominent perivascular signal (arrowhead) than observed with antibodies against AQP4. Kir4.1 immunoreactivity in hippocampus (f) and corpus (h) callosum of Aqp4−/− mice was similar to that of wild types. Scale bar 100 µm
Mentions: AQP4 immunofluorescence of immersion fixed tissue slices revealed a reticular labeling pattern compatible with staining of astrocytic processes in both hippocampus (Fig. 1a) and corpus callosum (Fig. 1c). Intense labeling was observed around blood vessels. Absence of AQP4 labeling in Aqp4−/− mice confirmed the selectivity of antibodies (Fig. 1e, g). Kir4.1 immunoreactivity in wild type animals resembled that of AQP4, but the signal was weaker around vessels (Fig. 1b, d). Importantly, the pattern of Kir4.1 immunoreactivity in hippocampus and corpus callosum was unaffected by Aqp4 deletion (Fig. 1f, h). The distribution of AQP4 and Kir4.1 labeling of immersion fixed slices was similar to that of perfusion fixed tissue (cf. Haj-Yasein et al. 2011).Fig. 1

Bottom Line: We show that Aqp4 deletion has a layer-specific effect on [K(+)]o that precisely mirrors the known effect on extracellular volume dynamics.In stratum pyramidale and corpus callosum, neither peak [K(+)]o nor post-stimulus [K(+)]o recovery was affected by Aqp4 deletion.Our data suggest that AQP4 modulates [K(+)]o during synaptic stimulation through its effect on extracellular space volume.

View Article: PubMed Central - PubMed

Affiliation: Letten Centre, Institute of Basic Medical Sciences, University of Oslo, 0317, Oslo, Norway.

ABSTRACT
The coupling between the water channel aquaporin-4 (AQP4) and K(+) transport has attracted much interest. In this study, we assessed the effect of Aqp4 deletion on activity-induced [K(+)]o changes in acute slices from hippocampus and corpus callosum of adult mice. We show that Aqp4 deletion has a layer-specific effect on [K(+)]o that precisely mirrors the known effect on extracellular volume dynamics. In CA1, the peak [K(+)]o in stratum radiatum during 20 Hz stimulation of Schaffer collateral/commissural fibers was significantly higher in Aqp4 (-/-) mice than in wild types, whereas no differences were observed throughout the [K(+)]o recovery phase. In stratum pyramidale and corpus callosum, neither peak [K(+)]o nor post-stimulus [K(+)]o recovery was affected by Aqp4 deletion. Our data suggest that AQP4 modulates [K(+)]o during synaptic stimulation through its effect on extracellular space volume.

No MeSH data available.


Related in: MedlinePlus