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2008 ; 82
(4
): 1748-58
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Hippocampal poly(ADP-Ribose) polymerase 1 and caspase 3 activation in neonatal
bornavirus infection
#MMPMID18057239
Williams BL
; Hornig M
; Yaddanapudi K
; Lipkin WI
J Virol
2008[Feb]; 82
(4
): 1748-58
PMID18057239
show ga
Infection of neonatal rats with Borna disease virus results in a characteristic
behavioral syndrome and apoptosis of subsets of neurons in the hippocampus,
cerebellum, and cortex (neonatal Borna disease [NBD]). In the NBD rat
hippocampus, dentate gyrus granule cells progressively degenerate. Apoptotic loss
of granule cells in NBD is associated with accumulation of zinc in degenerating
neurons and reduced zinc in granule cell mossy fibers. Excess zinc can trigger
poly(ADP-ribose) polymerase 1 (PARP-1) activation, and PARP-1 activation can
mediate neuronal death. Here, we evaluate hippocampal PARP-1 mRNA and protein
expression levels, activation, and cleavage, as well as apoptosis-inducing factor
(AIF) nuclear translocation and executioner caspase 3 activation, in NBD rats.
PARP-1 mRNA and protein levels were increased in NBD hippocampi. PARP-1
expression and activity were increased in granule cell neurons and glia with
enhanced ribosylation of proteins, including PARP-1 itself. In contrast, levels
of poly(ADP-ribose) glycohydrolase mRNA were decreased in NBD hippocampi. PARP-1
cleavage and AIF expression were also increased in astrocytes in NBD hippocampi.
Levels of activated caspase 3 protein were increased in NBD hippocampi and
localized to nuclei, mossy fibers, and dendrites of granule cell neurons. These
results implicate aberrant zinc homeostasis, PARP-1, and caspase 3 activation as
contributing factors in hippocampal neurodegeneration in NBD.