Retinal glial cells

Abstract

Müller cells, the principal glial cells of the retina of all vertebrates, were discovered already in 1851 but it was only in the past decades that it became evident that these cells are essential players in vision. Müller cells constitute the ‘core’ of columnar units of clonally and functionally related groups of neurons. 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). It has been shown 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 after neuronal excitation. 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. As another case of glial homeostasis, the maintenance of appropriate microenvironmental biomechanics has recently been described. Normal glial cells are softer than the neurons, and thus provide a suitable substrate for neurite growth during development, and for functional plasticity. Finally it should be pointed out that Müller cells are capable of ‘sensing’ neuronal activity. They respond to physiological light stimulation of their adjacent photoreceptors with two distinct types of intracellular calcium rises. These calcium rises then may trigger the release of signal substances, incl. so‐called ‘gliotransmitters’, from Müller cells which thus even may modify neuronal signal processing in the retina (e.g., in cases of adaptation to bright light, as another mechanism to increase the signal‐to‐noise ratio of information processing in retina). In cases of reactive Müller cell gliosis, the dominant potassium conductance of the membrane is down‐regulated and an increased expression of intermediate filaments is associated with increasing stiffness of the glial cell processes, such that all above‐mentioned glial functions are impaired.