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Christine R. Rose

Intracellular ion signalling and neuron-glia interaction at central synapses

Maintenance of ion gradients across the plasma membrane is a fundamental property of living cells. In the nervous system, these ion gradients are the basis for electrical excitability and electrical signaling. In addition, ions act as intracellular second messengers, and dynamic changes in the cytosolic ion concentration regulate many cellular processes.

Astrocytes in the mouse brainFigure 1: Astrocytes in the mouse brain, double-stained against their intracellular filament GFAP and the astrocyte marker S100ß. Their perivascular endfeet nicely delineate a blood vessel.

A basic characteristic of animal cells is the maintenance of a steep inwardly directed electrochemical gradient for sodium. This is achieved by the action of the Na+/K+-ATPase, which pumps sodium ions out of the cell in exchange for potassium. In the nervous system, the sodium gradient energizes intracellular ion regulation and provides the basis for the generation of action potentials and excitatory postsynaptic currents of neurons. The sodium gradient also drives the reuptake and inactivation of transmitters such as glutamate, a task mainly achieved by glial cells. Because of its vital functional importance, the sodium concentration of both neurons and glial cells was classically thought to be kept under tight homeostatic control and at a stable level under physiological conditions.

This picture is, however, far too simplistic. Recent research from our lab has established that active neurons experience significant transient sodium increases upon excitatory synaptic transmission due to influx of sodium through glutamate-gated ion channels. Excitatory activity also evokes long-lasting sodium transients in astrocytes, a major class of glial cells of the vertebrate brain, which mainly arise due to sodium-dependent glutamate uptake. While there is no clear evidence for buffering nor specific binding proteins for sodium, the properties of such activity-related sodium transients are fundamentally different from those described for intracellular calcium signals. The functional consequences of sodium transients are manifold and are just coming into view. It has become clear, however, that intracellular sodium changes might serve as signals themselves, influencing and regulating important cellular functions and playing a role in neuron-glia interaction.

Sodium signals in the neuronal networkFigure 2: Activity-induced intracellular sodium transients in the mouse hippocampus. Epileptiform bursts result in highly synchronized sodium signals in the entire neuronal network (green cells and traces; upper part) and also include astrocytes (magenta; lower part).

The projects in our lab address this question using high resolution dynamic imaging combined with whole-cell patch-clamp recordings in tissue slices of the rodent brain. Moreover, we study the mechanisms and functional consequences of sodium dysbalance under different pathological conditions.

Please visit PubMed for further literature and references.


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