Effect of bax deletion on ethanol sensitivity in the neonatal rat cerebellum
Article first published online: 7 OCT 2005
Copyright © 2005 Wiley Periodicals, Inc.
Journal of Neurobiology
Volume 66, Issue 1, pages 95–101, January 2006
How to Cite
Heaton, M. B., Paiva, M., Madorsky, I., Siler-Marsiglio, K. and Shaw, G. (2006), Effect of bax deletion on ethanol sensitivity in the neonatal rat cerebellum. J. Neurobiol., 66: 95–101. doi: 10.1002/neu.20208
- Issue published online: 16 NOV 2005
- Article first published online: 7 OCT 2005
- Manuscript Accepted: 10 FEB 2005
- Manuscript Received: 30 NOV 2004
- NIAAA. Grant Numbers: AA12151, AA07561
- 1990. Alcohol-induced neuronal loss in developing rats: Increased brain damage with binge exposure. Alcohol Clin Exp Res 14: 107–118. , .
- 2001. Elimination of bax expression in mice increases cerebellar Purkinje cell numbers but not the number of granule cells. J Comp Neurol 436: 82–91. , , .
- 1979. Observations on degenerative changes of Purkinje cells during early development in mice and in normal and otocyst-deprived chickens. Anat Embryol (Berl) 158: 95–102. .
- 1997. Alcohol-induced Purkinje cell loss with a single binge exposure in neonatal rats: A stereological study of temporal windows of vulnerability. Alcohol Clin Exp Res 21: 738–744. , .
- 1993. The effects of the timing of ethanol exposure during the brain growth spurt on the number of cerebellar Purkinje and granule cell nuclear profiles. Alcohol Clin Exp Res 17: 610–622. , .
- 2000. Ethanol-induced alterations in the expression of neurotrophic factors in the developing rat central nervous system. Dev Brain Res 121: 97–107. , , , .
- 1999. Bcl-2 overexpression protects the neonatal cerebellum from ethanol neurotoxicity. Brain Res 817: 13–18. , , , , .
- 2003a. The role of neurotrophic factors, apoptosis-related proteins, and endogenous antioxidants in the differential temporal vulnerability of neonatal cerebellum to ethanol. Alcohol Clin Exp Res 27: 657–669. , , , , , .
- 2003b. Ethanol effects on neonatal rat cortex: Comparative analyses of neurotrophic factors, apoptosis-related proteins, and oxidative processes during vulnerable and resistant periods. Dev Brain Res 145: 249–262. , , , .
- 2002. Ethanol-mediated generation of reactive oxygen species in developing rat cerebellum. Neurosci Lett 334: 83–86. , , , .
- 1995. In utero ethanol exposure elicits oxidative stress in the rat fetus. Alcohol Clin Exp Res 19: 714–720. , , , .
- 2000. Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome. Science 287: 1056–1060. , , , , , , , , , , et al.
- 2002. Changes of bcl-2 and bax mRNA expressions in the ethanol-treated mouse brain. Nihon Arukoru Yakubutsu Igakkai Zasshi 37: 120–129. , , , , , .
- 1973. Recognition of the fetal alcohol syndrome in early infancy. Lancet 2: 999–1001. , .
- 2002. A bax-induced pro-oxidant state is critical for cytochrome c release during programmed neuronal death. J Neurosci 22: 6480–6490. , , , .
- 1995. Ethanol-induced teratogenesis: Free radical damage as a possible mechanism. Teratology 52: 128–136. , , .
- 2002. Time course and manner of Purkinje neuron death following a single ethanol exposure on postnatal day 4 in the developing rat. Neuroscience 114: 327–337. , , .
- 1995. Neurotrophic factors attenuate glutamate-induced accumulation of peroxides, elevation of intracellular Ca2+ concentration, and neurotoxicity and increase antioxidant enzyme activities in hippocampal neurons. J Neurochem 65: 1740–1751. , , , .
- 1990. Neonatal ethanol exposure: Functional alterations associated with cerebellar growth retardation. Neurotox Teratol 12: 15–22. , , .
- 1997. Bax deletion further orders the cell death pathway in cerebellar granule cells and suggests a caspase-independent pathway to cell death. J Cell Biol 139: 205–217. , , , , , , .
- 2001. Effects of prenatal exposure to ethanol on the expression of bcl-2, bax and caspase 3 in the developing rat cerebral cortex and thalamus. Brain Res 911: 71–81. , .
- 1999. Neonatal ethanol exposure alters bcl-2 family mRNA levels in the rat cerebellar vermis. Alcohol Clin Exp Res 23: 1251–1261. , , .
- 1993. Intragastric intubation of alcohol during postnatal development of rats result in selective cell loss in the cerebellum. Alcohol Clin Exp Res 17: 1275–1280. , , .
- 2002. The antiapoptotic protein bcl-x(l) prevents the cytotoxic effect of bax, but not bax-induced formation of reactive oxygen species, in kluyveromyces lactis. Microbiology 148: 2789–2795. , , , .
- 2000. Bax inactivation in lurcher mutants rescues cerebellar granule cells but not Purkinje cells or inferior olivary neurons. J Neurosci 20: 5339–5345. , , .
- 1998. Alcohol-induced Purkinje cell loss depends on developmental timing of alcohol exposure and correlates with motor performance. Dev Brain Res 105: 159–166. , , .
- 2002. Cell death, bcl-2, bax, and the cerebellum. Cerebellum 1: 277–287. .
- 2003. Ethanol-induced neuronal apoptosis in vivo requires bax in the developing mouse brain. Cell Death Differ 10: 1148–1155. , , , , , , , , .
- 1996. Increased cerebellar Purkinje cell numbers in mice overexpressing a human bcl-2 transgene. J Comp Neurol 374: 332–341. , , , , .