Muller glial cells ensheath all retinal neurons in vertebrate
retinae. There are a multitude of functional interactions between
neurons and Muller cells, including delivery of the light stimuli
to the photoreceptor cells in the inverted vertebrate retina, a
'metabolic symbiosis' with the neurons, and the processing of
visual information. Muller cells are also responsible for the
maintenance of the homeostasis of the retinal extracellular milieu
(ions, water, neuro-transmitter molecules, and pH). In vascularized
retinae, Muller cells may also be involved in the control of
angiogenesis, and the regulation of retinal blood flow. Virtually
every disease of the retina is associated with a reactive Muller
cell gliosis which, on the one hand, supports the survival of
retinal neurons but, on the other hand, may accelerate the progress
of neuronal degeneration:
Muller cells protect neurons via a release of neurotrophic
factors. However, gliotic Muller cells display a dysregulation of
various neuron-supportive functions. This contributes to a
disturbance of retinal glutamate metabolism and ion homeostasis,
and causes the development of retinal edema and neuronal cell
death. Moreover, there are diseases evoking a primary Muller cell
insufficiency, such as hepatic retinopathy and certain forms of
glaucoma. Any impairment of supportive functions of Muller cells,
primary or secondary, must cause and/or aggravate a dysfunction and
loss of neurons, by increasing the susceptibility of neurons to
stressful stimuli in the diseased retina.
Muller cells may be used in the future for novel therapeutic
strategies to protect neurons against apoptosis (i.e. somatic gene
therapy), or to differentiate retinal neurons from Muller/stem
cells. Meanwhile, a proper understanding of the gliotic responses
of Muller cells in the diseased retina, and of their protective vs.
detrimental effects, is essential for the development of efficient
therapeutic strategies that use and stimulate the
neuron-supportive/-protective - and prevent the destructive -
mechanisms of gliosis.
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