Abstract

DO.09.01

Müller cells: basics in relation to disease

Andreas Reichenbach

Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig

Background and purpose

Müller cells are the principal glial cells of the retina. Similar as glial cells in other sensory organs and in the brain, their primary function is to support neuronal functioning (by increasing the signal-to-noise ratio of information processing) and survival (by maintaining a metabolic ‘symbiosis’ with the neurons). Much of this dual role of glial cells involves specific homeostatic mechanisms. Presently we are just beginning to understand what these mechanisms are, how they are organized and integrated simultaneously by a given cell, and how their impairment contributes to retinal malfunctioning and disease.
Method
Various experimental methods (electrophysiology, imaging methods, optical and biomechanical measurements) are employed to study glial cell functions in retina preparations from control animals and from diverse animal models of retinal diseases.
Results
We showed that Müller cells increase the signal-to-noise ratio of retinal information processing by, for instance, (i) guiding the light towards the photoreceptor cells, (ii) removing excess neurotransmitter molecules from extracellular space, and (iii) performing an efficient clearance of excess extracellular potassium ions. The latter two functions are also crucial for neuronal survival – to prevent excitotoxic effects of glutamate – and are coupled to water clearance which is equally important for neuronal survival. In cases of reactive Müller cell gliosis, the dominant potassium conductance of the membrane is down-regulated, and all above-mentioned glial functions are impaired. For instance, the impaired potassium homeostasis is associated with deficient water clearance; the cells swell and change their optical properties – i.e., lose their light guidance capability.
Conclusions
The gliotic decrease in K+ conductance may be a key event in the breakdown of glia-neuron interactions, triggering a severe (further) impairment of neuronal function and survival.

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