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Vol. 53, Issue 1, 33-42, January 1998
B Contributes to Excitotoxin-Induced Apoptosis
in Rat Striatum
Experimental Therapeutics Branch, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, Maryland 20892
Excitotoxin-induced destruction of striatal neurons, proposed as a
model of Huntington's disease, involves a process having the
biochemical stigmata of apoptosis. Recent studies suggested that
transcription factor nuclear factor (NF)-
B may be involved in
excitotoxicity. To further analyze the contribution of NFB to
excitotoxic neuronal death in vivo, changes in binding
activities of NFB and other transcription factors as well as the
consequences of inhibiting NFB nuclear translocation were measured
after the infusion of quinolinic acid (120 nmol) into rat striatum.
Internucleosomal DNA fragmentation and terminal transferase-mediated
dUTP digoxigenin nick end labeling-positive nuclei appeared 12 hr later
and intensified over the next 12 hr. NFB binding activity increased
severalfold from 2 to 12 hr, then gradually declined during the next 12 hr. Other transcription factor changes included AP-1, whose binding peaked about 6 hr after quinolinic acid administration, and E2F-1, which was only modestly and transiently elevated. In contrast, quinolinic acid lead to a reduction in OCT-1, beginning after 12 hr,
and briefly in SP-1 binding. The NFB, AP-1, and OCT-1 changes were
attenuated both by the N-methyl-D-aspartate
receptor antagonist MK-801 and the protein synthesis inhibitor
cycloheximide. Moreover, quinolinic acid-induced internucleosomal DNA
fragmentation and striatal cell death were significantly reduced by the
intrastriatal administration of NFB SN50, a cell-permeable
recombinant peptide that blocks NFB nuclear translocation. These
results illustrate the complex temporal pattern of transcription factor
change attending the apoptotic destruction produced in rat striatum by
quinolinic acid. They further suggest that NFB activation
contributes to the excitotoxin-induced death of striatal neurons.
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