Abstract：
:In contrast to its known anti-apoptotic activity in sympathetic neurons, immortal neuronal cell lines, and primary cultured immature neurons of the central nervous system (CNS), the role of Bcl-2 in CNS neurons in the adult brain is poorly understood. In the present study, we examined effects of overexpression of Bcl-2 on selective neuronal death of the hippocampal CA1 neurons and the dentate granule cells induced by hypoxic ischemia in adult transgenic mice overexpressing human Bcl-2 under the control of neuron-specific enolase (NSE-hbcl-2). At the light microscopic level, numbers of TUNEL-positive cells with pyknotic nuclei were observed in the CA1 subfield of NSE-hbcl-2 transgenic mice, as well as that of wild-type mice, after hypoxic ischemic insult, although the onset of neuronal death was apparently delayed in NSE-hbcl-2 transgenic mice. The electron microscopic studies showed that morphological changes of the degenerating CA1 neurons from both groups were clearly distinct from ordinary apoptosis. In contrast, a significant amount of degenerating dentate granule cells from wild-type but not from transgenic mice had typical apoptotic nuclei by the treatment. The activation of caspase-3 was detected in the dentate granule cells but not that of the CA1 neurons. These results indicate that the overexpression of Bcl-2 effectively suppressed dentate granule cell apoptosis but only delayed cell death of the CA1 neurons induced by hypoxic ischemia, suggesting the occurrence of a non-apoptotic, caspase-3-independent mechanism for neuronal death in the CA1 subfield.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Wang HD,Fukuda T,Suzuki T,Hashimoto K,Liou SY,Momoi T,Kosaka T,Yamamoto K,Nakanishi Hdoi
10.1002/(SICI)1097-4547(19990701)57:1<1::AID-JNR1>keywords:
subject
Has Abstractpub_date
1999-07-01 00:00:00pages
1-12issue
1eissn
0360-4012issn
1097-4547pii
10.1002/(SICI)1097-4547(19990701)57:1<1::AID-JNR1>journal_volume
57pub_type
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