Apoptosis in Neurobiology (Frontiers in Neuroscience)
Language: English
Pages: 296
ISBN: 0849333520
Format: PDF / Kindle (mobi) / ePub
The rapid growth of the study of apoptosis-mechanism-driven, regulated cell death-has created an urgent need for reliable documentation of the different approaches to and methods of studying the various aspects of the field. Apoptosis in Neurobiology is an important resource for researchers in this emerging frontier of biomedical study. This volume allows the uninitiated neuroscientist intellectual and practical access to the study of apoptosis, with special consideration to the nervous system. The first section concentrates on conceptual approaches to the study of apoptosis in neurobiology and its significance to the nervous system. The second section provides a user-friendly approach to methods and techniques in the study of apoptosis as applied to neurobiology.
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Responsible gene, CLN3 on chromosome 16, which has been cloned and sequenced.30 Recent work shows that the 438-amino acid protein product of this gene is operative in a novel antiapoptotic pathway. The CLN3 peptide modulates both endogenous and vincristine stimulated levels of ceramide suggesting mediation of its antiapoptotic effect by attenuating ceramide levels. The human disease is associated with deletions of the CLN3 gene, which apparently result in loss of function. The gene defect in.
Ophthalmol. Vis. Sci., 35, 4182, 1994. 38. Portera-Cailliau, C., Sung, C. H., Nathans J., and Adler R., Apoptotic photoreceptor cell death in mouse models of retinitis pigmentosa, Proc. Natl. Acad. Sci. U.S.A., 91, 974, 1994. 39. Lolley, R. N., Rong, H., and Craft, C. M., Linkage of photoreceptor degeneration by apoptosis with inherited defect in phototransduction, Invest. Ophthalmol. Vis. Sci., 35, 358, 1994. 40. Tso, M. O., Zhang, C., Abler, A. S., Chang, C. J., Wong, F., Chang, G. Q. and Lam,.
Novel methods by which to target nervous system neoplasia for apoptosis induction are discussed in this section. © 1999 by CRC Press LLC The hydroxymethylglutaryl- (HMG-) CoA reductase inhibitor, lovastatin, has been reported to have a differential apoptosis-inducing effect upon glioma cells, as opposed to normal glial cells in culture.33,34 In glioma cells, this drug induces growth arrest followed by apoptosis.35 In normal glial cells, only a reversible decrease in the rate of DNA synthesis.
Juvenile Batten disease (JNCL) were subjected to TUNEL staining using the ApopTag kit from Oncor (Gaithersburg, MD).50,51 Apoptotic cells are identifiable as those containing brown nuclei; normal nuclei stain blue. Figure 8.2 shows the results from a TUNEL staining experiment with indirect fluorescent detection. A human brain tissue section (treated with DNaseI to artificially induce DNA fragmentation) was labeled with digoxigenin-dUTP and then visualized by addition of a rhodamine-conjugated.
A study of delayed neuronal degeneration in carbon monoxide exposure.13 In Table 9.1, a list of nuclear changes is given for the spectrum between apoptosis and necrosis.1-4,11,13,31,32 In addition, one must consider in nervous © 1999 by CRC Press LLC FIGURE 9.1 © 1999 by CRC Press LLC tissue the occurrence of cells altered during postmortem fixation such as “dark neurons” and other neuronal changes such as retrograde reaction after axonal injury.14,18,19 The application of these criteria is.