Christine R. Rose
Heinrich Heine University Düsseldorf
Intracellular ion signalling in the vertebrate brain, its cellular pathways, and its functional consequences under physiological as well as pathophysiological conditions. Dynamic high-resolution imaging, such as multi-photon laser scanning microscopy. Various electrophysiological techniques in both neurons and glial cells of the mouse brain in situ.
Vita
since 2005 | Full professor and head of the Institute of Neurobiology at Heinrich-Heine-Universität Düsseldorf |
2003-2005 | Heisenberg fellowship of the DFG, Department of Physiology, Technische Universität and Ludwig-Maximilians-Universität München |
2002 | Professional dissertation (Habilitation) in Physiology, Ludwig-Maximilians-Universität, München |
2000-2003 | Postdoc at Department of Physiology, Technische Universität and Ludwig-Maximilians-Universität München |
1997-1999 | Postdoc at Department of Physiology, Medical faculty, Universität des Saarlandes, Homburg |
1994-1997 | Postdoc at Department of Neurology, Yale University School of Medicine, New Haven, CT, USA |
1993 | Dissertation (Dr. rer. nat.) at University of Kaiserslautern |
1990 | Diploma in Biology at University of Konstanz |
Research
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.
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.
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.
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