Functional and molecular interactions between aquaporins and Na,K-ATPase

Illarionova, N. B.; Gunnarson, Eli; Li, Y.; Brismar, Hjalmar; Bondar, Alexander A.; Zelenin, Sergey; Aperia, Anita

doi:10.1016/j.neuroscience.2009.11.062

Cited by 82 publications

(62 citation statements)

References 199 publications

(181 reference statements)

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“…tion because both molecules form macromolecular complexes in astrocytes and probably functionally interact with each other (Illarionova et al, 2010). The neuronal Na 1 /K 1 -ATPase seems not to be impaired in AQP4 2/2 mice because we observed similar amplitudes of the undershoot as in wt mice (Heinemann and Lux, 1975;Ransom et al, 2000).…”

Section: Discussionsupporting

confidence: 49%

Impact of aquaporin‐4 channels on K⁺ buffering and gap junction coupling in the hippocampus

Strohschein¹,

Hüttmann²,

Gabriel³

et al. 2011

Glia

147

146

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Aquaporin-4 (AQP4) is the main water channel in the brain and primarily localized to astrocytes where the channels are thought to contribute to water and K(+) homeostasis. The close apposition of AQP4 and inward rectifier K(+) channels (Kir4.1) led to the hypothesis of direct functional interactions between both channels. We investigated the impact of AQP4 on stimulus-induced alterations of the extracellular K(+) concentration ([K(+)](o)) in murine hippocampal slices. Recordings with K(+)-selective microelectrodes combined with field potential analyses were compared in wild type (wt) and AQP4 knockout (AQP4(-/-)) mice. Astrocyte gap junction coupling was assessed with tracer filling during patch clamp recording. Antidromic fiber stimulation in the alveus evoked smaller increases and slower recovery of [K(+)](o) in the stratum pyramidale of AQP4(-/-) mice indicating reduced glial swelling and a larger extracellular space when compared with control tissue. Moreover, the data hint at an impairment of the glial Na(+)/K(+) ATPase in AQP4-deficient astrocytes. In a next step, we investigated the laminar profile of [K(+)](o) by moving the recording electrode from the stratum pyramidale toward the hippocampal fissure. At distances beyond 300 μm from the pyramidal layer, the stimulation-induced, normalized increases of [K(+)](o) in AQP4(-/-) mice exceeded the corresponding values of wt mice, indicating facilitated spatial buffering. Astrocytes in AQP4(-/-) mice also displayed enhanced tracer coupling, which might underlie the improved spatial re- distribution of [K(+)](o) in the hippocampus. These findings highlight the role of AQP4 channels in the regulation of K(+) homeostasis.

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Section: Discussionsupporting

confidence: 49%

Impact of aquaporin‐4 channels on K⁺ buffering and gap junction coupling in the hippocampus

Strohschein¹,

Hüttmann²,

Gabriel³

et al. 2011

Glia

147

146

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“…Although the exact mechanism was not determined, NO is known to inhibit Na + /K + -ATPase [45,46]. This inhibition may cause an increase in intracellular sodium, leading to water influx through AQP4 [47]. NO is known to increase in the brain as a result of various insults which include traumatic injury [22], ischemia [20], and inflammatory degeneration [21].…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Increases the Expression of Aquaporin-4 Protein in Rat Optic Nerve Astrocytes through the Cyclic Guanosine Monophosphate/Protein Kinase G Pathway

et al. 2015

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Aims: Nitric oxide (NO) is associated with neuroinflammation in the central nervous system. We determined whether NO increases the expression of aquaporin-4 (AQP4) in optic nerve astrocytes of rats. Methods: Isolated astrocytes were incubated under normoxic or hypoxic conditions with or without glucose (5.5 mM). The astrocytes were also exposed to different concentrations of S-nitroso-N-acetyl-DL-penicillamine (SNAP, 1.0-100 μM), an NO donor. The expression of AQP4 was determined by Western blot analyses, and NO formation was measured by the Griess reaction. The changes in astrocytic cellular volumes were determined by flow cytometry. Results: Hypoxia and glucose deprivation increased AQP4 expression and NO formation. Inhibition of NO synthetase (NOS) significantly suppressed these changes. SNAP caused a significant increase in AQP4 expression, and the increase was significantly suppressed by carboxy-PTIO, a scavenger of NO. Incubation with 8-Br-cyclic guanosine monophosphate (cGMP) mimicked the effects of SNAP, while the addition of either 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ; inhibitor of soluble guanylate cyclase) or KT5823 (protein kinase G inhibitor) suppressed the SNAP-induced increase in AQP4 significantly. SNAP also caused a significant increase in astrocytic cellular volume through the AQP4 channels. Conclusions: NO increased the AQP4 expression of optic nerve astrocytes through the cGMP/protein kinase G pathway and enlarged their volume.

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“…Possibly, the subset of ventral CNS regions that express both Atp1a3a and Atp1a3b involves a pathological pathway that results in this phenotype A functional Na ϩ /K ϩ -ATPase, in a complex with aquaporins and glutamate transporters, and is important for maintaining water and ion balance in the brain (42). Interestingly, Na ϩ /K ϩ -ATPase, in particular Atp1a1, was previously demonstrated to be required for the zebrafish brain ventricle development (19,43).…”

Section: Discussionmentioning

confidence: 99%

α3Na+/K+-ATPase Deficiency Causes Brain Ventricle Dilation and Abrupt Embryonic Motility in Zebrafish

Doğanlı

Beck

Ribera

et al. 2013

Journal of Biological Chemistry

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Functional and molecular interactions between aquaporins and Na,K-ATPase

Cited by 82 publications

References 199 publications

Impact of aquaporin‐4 channels on K⁺ buffering and gap junction coupling in the hippocampus

Impact of aquaporin‐4 channels on K⁺ buffering and gap junction coupling in the hippocampus

Nitric Oxide Increases the Expression of Aquaporin-4 Protein in Rat Optic Nerve Astrocytes through the Cyclic Guanosine Monophosphate/Protein Kinase G Pathway

α3Na+/K+-ATPase Deficiency Causes Brain Ventricle Dilation and Abrupt Embryonic Motility in Zebrafish

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Functional and molecular interactions between aquaporins and Na,K-ATPase

Cited by 82 publications

References 199 publications

Impact of aquaporin‐4 channels on K+ buffering and gap junction coupling in the hippocampus

Impact of aquaporin‐4 channels on K+ buffering and gap junction coupling in the hippocampus

Nitric Oxide Increases the Expression of Aquaporin-4 Protein in Rat Optic Nerve Astrocytes through the Cyclic Guanosine Monophosphate/Protein Kinase G Pathway

α3Na+/K+-ATPase Deficiency Causes Brain Ventricle Dilation and Abrupt Embryonic Motility in Zebrafish

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Impact of aquaporin‐4 channels on K⁺ buffering and gap junction coupling in the hippocampus

Impact of aquaporin‐4 channels on K⁺ buffering and gap junction coupling in the hippocampus