Who's on first … Na+, HCO3− or CO32−?

Romero, Michael F.

doi:10.1113/jp282945

Cited by 2 publications

(1 citation statement)

References 8 publications

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“…At more severe decreases in pH i ; e.g., those accompanying severe ischemia, the Na +/ H + exchanger NHE1 is central for the export of protons [18,60,61]. The stoichiometry of NBCe1 in the forward mode is 1Na + :2HCO 3 − [57,62,63], while in the reverse mode, it has recently been demonstrated to transport 1Na + :1HCO 3 − :1CO 3 2− [64,65]. In physiological conditions, the reversal potential of NBCe1 is close to the typical resting membrane potential of forebrain astrocytes (about −85 mV; see, e.g., [41]).…”

Section: Nbce1 Activity Influences Astrocytic Ph I and [Na + ] Imentioning

confidence: 99%

Inward Operation of Sodium-Bicarbonate Cotransporter 1 Promotes Astrocytic Na+ Loading and Loss of ATP in Mouse Neocortex during Brief Chemical Ischemia

Everaerts,

Thapaliya,

Pape

et al. 2023

Cells

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Ischemic conditions cause an increase in the sodium concentration of astrocytes, driving the breakdown of ionic homeostasis and exacerbating cellular damage. Astrocytes express high levels of the electrogenic sodium-bicarbonate cotransporter1 (NBCe1), which couples intracellular Na+ homeostasis to regulation of pH and operates close to its reversal potential under physiological conditions. Here, we analyzed its mode of operation during transient energy deprivation via imaging astrocytic pH, Na+, and ATP in organotypic slice cultures of the mouse neocortex, complemented with patch-clamp and ion-selective microelectrode recordings and computational modeling. We found that a 2 min period of metabolic failure resulted in a transient acidosis accompanied by a Na+ increase in astrocytes. Inhibition of NBCe1 increased the acidosis while decreasing the Na+ load. Similar results were obtained when comparing ion changes in wild-type and Nbce1-deficient mice. Mathematical modeling replicated these findings and further predicted that NBCe1 activation contributes to the loss of cellular ATP under ischemic conditions, a result confirmed experimentally using FRET-based imaging of ATP. Altogether, our data demonstrate that transient energy failure stimulates the inward operation of NBCe1 in astrocytes. This causes a significant amelioration of ischemia-induced astrocytic acidification, albeit at the expense of increased Na+ influx and a decline in cellular ATP.

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Section: Nbce1 Activity Influences Astrocytic Ph I and [Na + ] Imentioning

confidence: 99%

Inward Operation of Sodium-Bicarbonate Cotransporter 1 Promotes Astrocytic Na+ Loading and Loss of ATP in Mouse Neocortex during Brief Chemical Ischemia

Everaerts,

Thapaliya,

Pape

et al. 2023

Cells

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Evolving views of ionic, osmotic and acid–base regulation in aquatic animals

Tresguerres

Kwan

Weinrauch

2023

Journal of Experimental Biology

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The regulation of ionic, osmotic and acid–base (IOAB) conditions in biological fluids is among the most fundamental functions in all organisms; being surrounded by water uniquely shapes the IOAB regulatory strategies of water-breathing animals. Throughout its centennial history, Journal of Experimental Biology has established itself as a premier venue for publication of comparative, environmental and evolutionary studies on IOAB regulation. This Review provides a synopsis of IOAB regulation in aquatic animals, some of the most significant research milestones in the field, and evolving views about the underlying cellular mechanisms and their evolutionary implications. It also identifies promising areas for future research and proposes ideas for enhancing the impact of aquatic IOAB research.

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Who's on first … Na⁺, HCO₃⁻ or CO₃²⁻?

Cited by 2 publications

References 8 publications

Inward Operation of Sodium-Bicarbonate Cotransporter 1 Promotes Astrocytic Na+ Loading and Loss of ATP in Mouse Neocortex during Brief Chemical Ischemia

Inward Operation of Sodium-Bicarbonate Cotransporter 1 Promotes Astrocytic Na+ Loading and Loss of ATP in Mouse Neocortex during Brief Chemical Ischemia

Evolving views of ionic, osmotic and acid–base regulation in aquatic animals

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