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Localization of Bcl-xβ in the developing and adult rat central nervous system
bcl‐xβ is a novel apoptosis‐regulating member of the bcl‐x family that has recently been isolated from rats and mice. To explore the functional role of Bcl‐xβ, we raised a monoclonal antibody against rat Bcl‐xβ protein and investigated the cellular localization of the molecule in the rat CNS. Immuno...
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Published in: | Journal of neuroscience research 2000-05, Vol.60 (4), p.468-477 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | bcl‐xβ is a novel apoptosis‐regulating member of the bcl‐x family that has recently been isolated from rats and mice. To explore the functional role of Bcl‐xβ, we raised a monoclonal antibody against rat Bcl‐xβ protein and investigated the cellular localization of the molecule in the rat CNS. Immunohistochemistry revealed that, in the fetal and neonatal stages, Bcl‐xβ was intensively and widely expressed in the CNS. Many neurons in the diencephalon and brain stem showed intense cytoplasmic labeling. The immunoreactivity decreased during the postnatal development and reached to the level of adulthood by P14. In the adult brain and spinal cord, labeling was restricted to specific types of neurons and distributed throughout their somata and dendrites. Weak immunoreactivity was present in many CNS regions such as the cerebral cortex, hippocampal dentate gyrus, caudate‐putamen, globus pallidus, thalamus, locus ceruleus, pontine nuclei, inferior olive, reticular formation, cerebellar cortex and spinal anterior horn. Amygdaloid nuclei and hippocampal CA1 to CA3 sectors showed restricted expression of Bcl‐xβ in a subset of neurons. Neuronal labeling was almost undetectable in several regions, including the piriform cortex, hypothalamus, posterior column nuclei and spinal posterior horn. These results suggest that Bcl‐xβ plays an important role throughout the CNS in developing stage and may regulate the apoptosis of postnatal CNS neurons. J. Neurosci. Res. 4:468–477, 2000 © 2000 Wiley‐Liss, Inc. |
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ISSN: | 0360-4012 1097-4547 |
DOI: | 10.1002/(SICI)1097-4547(20000515)60:4<468::AID-JNR5>3.0.CO;2-V |