Alterations in the fine structure of nucleoli in sympathetic neurons following NGF-antiserum treatment
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Cited by (39)
Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain
2008, Neurobiology of DiseaseCitation Excerpt :To the best of our knowledge, there are no prior studies demonstrating in the in vivo developing brain that lithium stimulates ERK phosphorylation or that increased phosphorylation of ERK is protective against drug-induced developmental neuroapoptosis. The neuroapoptosis literature is massive, but models for inducing apoptotic neurodegeneration in the in vivo developing nervous system are scarce, the two best characterized examples being the phenomenon under investigation herein, and degeneration of sympathetic neurons induced by trophic factor deprivation, as originally described by Levi-Montalcini et al. (1969) and others (Sabatini et al., 1965). As Dikranian et al. (2001, 2005) recently pointed out, these two phenomena have identical ultrastructural characteristics and both meet all of the morphological criteria originally stipulated by Wyllie et al. (1980) for recognizing apoptosis.
Ethanol-induced neuroapoptosis in the developing rodent cerebellum and related brain stem structures
2005, Developmental Brain ResearchRescue of NGF-deficient mice I: Transgenic expression of NGF in skin rescues mice lacking endogenous NGF
2004, Molecular Brain ResearchEthanol-induced apoptotic neurodegeneration in the developing C57BL/6 mouse brain
2002, Developmental Brain ResearchApoptosis in the in vivo mammalian forebrain
2001, Neurobiology of DiseaseDistinct alterations in mitochondrial mass and function characterize different models of apoptosis
1998, Experimental Cell Research
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Permanent address: Istituto di Patologia Generale, Universita´di Roma, Rome, Italy.