Apoptosis, or programmed cell death, involves a cascade of regulatory events leading to the activation of specific proteases. However, the key substrates for these proteases remain to be identified. We previously demonstrated that levels of five unidentified polypeptides were specifically increased in neurons from embryonic chicken ciliary ganglia undergoing apoptosis by trophic deprivation.
View Article and Find Full Text PDFRecent studies have revealed that proteins such as growth-associated protein 43 (GAP-43) and neuron-specific enolase (NSE), believed for many years to be expressed exclusively in neurons, are also present in glial cells under some circumstances. Here we present an overview of these observations. GAP-43 is expressed both in vitro and in vivo transiently in immature rat oligodendroglial cells of the central nervous system, in Schwann cell precursors, and in non-myelin-forming Schwann cells of the peripheral nervous system.
View Article and Find Full Text PDFA series of substances (designated CTQ compounds) with a guanidine group have been synthesized and tested for their ability to promote neuronal survival and neurite outgrowth. Mouse neuroblastoma clonal cell lines grown in serum-containing medium for 10 days as well as primary cultures of embryonic chicken ganglion neurons grown in serum-free defined medium for 1 or 2 days have been used for the experiments. Among the various CTQ compounds (CTQ1-CTQ20) tested, only CTQ8 exerted positive neurotrophic effects on these peripheral neuronal cells.
View Article and Find Full Text PDFWe report the presence and distribution of alpha (ubiquitous) and gamma (neuron-specific) subunits of the dimeric glycolytic enzyme enolase (2-phospho-D-glycerate hydrolase) in cultured neural cells. The gamma gamma enolase is found in vivo at high levels only in neurons and neuroendocrine cells. Neuronal cells in culture also contain relatively high levels of alpha gamma and gamma gamma enolase.
View Article and Find Full Text PDFReactive gliosis is a reaction of glial cells to trauma which is characterized by a phenotypic modification of astrocytes, as well as by a proliferation and a migration of some of these cells to form a glial scar. This scar is currently considered as a physical impediment to neuronal regrowth but it may also be involved in wound healing since the astrocytes beside microglia play a phagocytic role in the clearance of post-traumatic debris. Growth factors are released in the area of the injury and at least some of them could be involved in gliosis.
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