Background. Satellites are glial cells adherent to neuronal somata, a phenomenon known as satellitosis. Such glia are both astrocytes and oligodendrocytes. A few occur normally, but are increased in a variety of encephalopathies including epilepsy. Their significance is unknown, but opposing hypotheses assert that they are neuroprotective chaperones or that they are neurotoxic. Satellitosis often is dismissed as nonspecific, hence unimportant.Materials and Methods: From November 2004 to April 2010 we examined 28 resections of temporal neocortex and hippocampus for epilepsy in children. Histo-pathological diagnoses were focal cortical dysgenesis, mesial temporal sclerosis or histologically normal. Tumours were excluded. Immunocytochemical markers and electron micoscopy were performed in all.Results: Multiple glial cells surrounded the soma of some pyramidal neurons in both neocortex and Ammon's horn in all cases. Ultrastructure confirmed satellitosis of preserved neurons, but also demonstrated excessive but intact glial cells adherent to degenerating neurons. The dying neurons were not felt to be the "dark neurons" of light microscopy seen in some metabolic encephalopathies and or tissue artifacts. Scattered degenerating myelinated axons were demonstrated in white matter.Conclusions: We propose a mechanism in which 1) satellites displace axonal terminals of inhibitory axosomatic synapses, resulting in shift in equilibrium between excitation and inhibition, enhancing epileptogenic neurons initially and later contributing to their death. 2) Astrocytic biosynthesis of glutamine may transport excess glutamine to neurons to be converted to intraneuronal neurotoxic glutamate. 3) Extracellular matix molecules secreted by glial cells can render neuronal membranes more easily depolarized. Satellite glial cells thus contribute both to epileptogenesis and to neuronal death, hence are not neuroprotective.
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