Abstract
Bilirubin encephalopathy (BE), which includes acute (kernicterus) and chronic (postkernicteric)
forms, results from severe neonatal jaundice. In order to investigate neurodegenerative
mechanisms in autopsy cases of BE, we immunohistochemically examined expressions of
neurotransmitters, neuropeptides, and calcium-binding proteins in the basal ganglia;
and deposition of oxidative products. Expression of tyrosine hydroxylase was reduced
in the putamen in cases of acute BE, and in the globus pallidus in cases of acute
and chronic postkernicteric BE. Methionine–enkephalin expression was reduced in the
external segment of the globus pallidus in cases of acute and chronic postkernicteric
BE, and immunoreactivity for substance P was severely altered in both internal and
external segments in cases of chronic postkernicteric BE. A decrease in the number
of parvalbumin-immunoreactive interneurons in the external segment of the globus pallidus
was observed predominantly in cases of acute BE, whereas the number of interneurons
immunoreactive for calbindin-D28K was reduced in the putamen in cases of chronic postkernicteric
BE. Nuclear immunoreactivity for 8-hydroxy-2′-deoxyguanosine was seen in the putamen
in half of the BE cases. These findings indicated that the putamen was impaired in
BE and the pallidal external segment was also damaged in the acute form of BE, suggesting
that oxidative damage to DNA is implicated in lesions of the basal ganglia.
Keywords
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Article info
Publication history
Accepted:
August 29,
2007
Received in revised form:
August 27,
2007
Received:
April 27,
2007
Identification
Copyright
© 2007 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
