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Vol. 286, Issue 1, 539-547, July 1998
Section on Molecular Neurobiology, Biological Psychiatry Branch,
National Institute of Mental Health, National Institutes of Health,
Bethesda, Maryland (S.N. and D.-M.C.);
Minase Research Institute, Ono
Pharmaceutical Co., Ltd., Osaka, Japan (N.K.)
We have studied the neuroprotective actions of lithium against various
insults in cultured cerebellar granule cells of rats. The
anticonvulsants, phenytoin and carbamazepine, have been shown to induce
apoptosis of cerebellar granule cells at high concentrations. Here we
found that co-presence of LiCl (1-10 mM) dose-dependently protected
against phenytoin (20 µM)- and carbamazepine (100 µM)-induced neuronal apoptosis as assessed by
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide
metabolism, morphological inspection, chromatin condensation and DNA
fragmentation. These neuroprotective effects were not prevented by
inclusion of myoinositol nor mimicked by a potent inositol
monophosphatase inhibitor, suggestive of a mechanism independent of
inositol monophosphatase blockade. Lithium also significantly protected
against apoptosis of cerebellar granule cells induced by aging of the
cultures. Additionally, lithium suppressed death of cerebellar granule
cells exposed to a low concentration of extracellular potassium. In
contrast, it had no protective effect on cell death induced by
Ca++ ionophores, a Na+ channel opener, a
protein kinase inhibitor, a nitric oxide donor or
H2O2. Thus, lithium has robust neuroprotective
effects against apoptotic cell death induced by multiple insults with
limited selectivity. These actions provide a new avenue to study the
molecular and cellular mechanisms of this drug.
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