Correction: Felix, L.; Ziemens, D.; Seifert, G.; Rose, C.R. Spontaneous Ultraslow Na Fluctuations in the Neonatal Mouse Brain. 2020, , 102.

The authors wish to make the following changes to their paper [...

Spontaneous Ultraslow Na Fluctuations in the Neonatal Mouse Brain.

In the neonate forebrain, network formation is driven by the spontaneous synchronized activity of pyramidal cells and interneurons, consisting of bursts of electrical activity and intracellular Ca oscillations. By employing ratiometric Na imaging in tissue slices obtained from animals at postnatal day 2-4 (P2-4), we found that 20% of pyramidal neurons and 44% of astrocytes in neonatal mouse hippocampus also exhibit transient fluctuations in intracellular Na. These occurred at very low frequencies (~2/h), were exceptionally long (~8 min), and strongly declined after the first postnatal week.

On the special role of NCX in astrocytes: Translating Na-transients into intracellular Ca signals.

As a solute carrier electrogenic transporter, the sodium/calcium exchanger (NCX1-3/SLC8A1-A3) links the trans-plasmalemmal gradients of sodium and calcium ions (Na, Ca) to the membrane potential of astrocytes. Classically, NCX is considered to serve the export of Ca at the expense of the Na gradient, defined as a "forward mode" operation. Forward mode NCX activity contributes to Ca extrusion and thus to the recovery from intracellular Ca signals in astrocytes.

Heterogeneity of Activity-Induced Sodium Transients between Astrocytes of the Mouse Hippocampus and Neocortex: Mechanisms and Consequences.

Activity-related sodium transients induced by glutamate uptake represent a special form of astrocyte excitability. Astrocytes of the neocortex, as opposed to the hippocampus proper, also express ionotropic glutamate receptors, which might provide additional sodium influx. We compared glutamate-related sodium transients in astrocytes and neurons in slices of the neocortex and hippocampus of juvenile mice of both sexes, using widefield and multiphoton imaging.

Molecular and cellular physiology of sodium-dependent glutamate transporters.

Glutamate is the major excitatory transmitter in the vertebrate brain. After its release from presynaptic nerve terminals, it is rapidly taken up by high-affinity sodium-dependent plasma membrane transporters. While both neurons and glial cells express these excitatory amino acid transporters (EAATs), the majority of glutamate uptake is accomplished by astrocytes, which convert synaptically-released glutamate to glutamine or feed it into their own metabolism.

Lactate rescues neuronal sodium homeostasis during impaired energy metabolism.

Recently, we established that recurrent activity evokes network sodium oscillations in neurons and astrocytes in hippocampal tissue slices. Interestingly, metabolic integrity of astrocytes was essential for the neurons' capacity to maintain low sodium and to recover from sodium loads, indicating an intimate metabolic coupling between the 2 cell types. Here, we studied if lactate can support neuronal sodium homeostasis during impaired energy metabolism by analyzing whether glucose removal, pharmacological inhibition of glycolysis and/or addition of lactate affect cellular sodium regulation.

Astrocytes restrict discharge duration and neuronal sodium loads during recurrent network activity.

Influx of sodium ions into active neurons is a highly energy-expensive process which must be strictly limited. Astrocytes could play an important role herein because they take up glutamate and potassium from the extracellular space, thereby dampening neuronal excitation. Here, we performed sodium imaging in mouse hippocampal slices combined with field potential and whole-cell patch-clamp recordings and measurement of extracellular potassium ([K(+)]o).