19 research outputs found
The role of brain-derived neurotrophic factor in the pathophysiology of adolescent suicidal behavior
Brain-derived neurotrophic factor prevents the death of motoneurons in newborn rats after nerve section
Motoneurons innervating the skeletal musculature were among the first neurons shown to require the presence of their target cells to develop appropriately. But the characterization of molecules allowing motoneuron survival has been difficult. Ciliary neurotrophic factor prevents the death of motoneurons, but its gene is not expressed during development. Although the presence of a neurotrophin receptor on developing motoneurons has suggested a role for neurotrophins, none could be shown to promote motoneuron survival in vitro. We report here that brain-derived neurotrophic factor can prevent the death of axotomized motoneurons in newborn rats, suggesting a role for this neurotrophin for motoneuron survival in vivo
Brain-derived neurotrophic factor prevents the death of motoneurons in newborn rats after nerve section
Validated HPLC and stability-indicating densitometric chromatographic methods for simultaneous determination of camylofin dihydrochloride and paracetamol in their binary mixture
Three important components in the regeneration of the cavernous nerve: brain-derived neurotrophic factor, vascular endothelial growth factor and the JAK/STAT signaling pathway
The neurotrophin receptor p75(NTR) : novel functions and implications for diseases of the nervous system
Neurotrophins have long been known to promote the survival and differentiation of vertebrate neurons. However, these growth factors can also induce cell death through the p75 neurotrophin receptor (p75(NTR)), a member of the tumor necrosis factor receptor superfamily. Consistent with a function in controlling the survival and process formation of neurons, p75(NTR) is mainly expressed during early neuronal development. In the adult, p75(NTR) is re-expressed in various pathological conditions, including epilepsy, axotomy and neurodegeneration. Potentially toxic peptides, including the amyloid beta- (Abeta-) peptide that accumulates in Alzheimer's disease, are ligands for p75(NTR). Recent work also implicates p75(NTR) in the regulation of both synaptic transmission and axonal elongation. It associates with the Nogo receptor, a binding protein for axonal growth inhibitors, and appears to be the transducing subunit of this receptor complex