Taehan Chŏngsin Yangmul Hakhoe chi; The Korean journal of psychopharmacology; 대한정신약물학회지
Objective：Several lines of evidence have shown that neuronal injury might represent a possible pathway to mood disorders. The present study was performed to examine the possibility that the neuroprotective effects of R(-)- and S(+)-citalopram depend on types of neuronal cell death.
Methods：Free radical neurotoxicity was induced in mixed cortical cell cultures by continuous exposure to 30 μM Fe++ for 24 hours, which produced hydroxyl radicals via a Fenton reaction. Cultures measuring excitotoxicity were exposed for 24 hours to 50 μM NMDA. Neuronal apoptosis was induced by 100 nM staurosporine exposure for 24 hours. Neuronal death was analyzed 24 hours later by measuring the efflux of lactate dehydrogenase (LDH) into the bathing medium or by counting viable neurons after staining with trypan blue.
Results：Co-treatment with R(-)-or S(+)-citalopram prevented staurosporine-induced apoptosis of cultured cortical cells, as well as activation of caspase-3. In contrast to the differences between enantiomers found in serotonin uptake inhibition and in the in vivo behavioral depression model, both enantiomers in this study showed similar protective effects on staurosporine-induced apoptosis. Mixed cortical cell cultures exhibited marked swelling of the neuronal cell bodies accompanied by widespread neuronal death during the 24 hours following exposure to 30 μM Fe++ or 50 μM NMDA that was not sensitive to either the R(-)-or S(+)-enantiomers of citalopram.
Conclusion：These features suggest that the neuroprotective effect of citalopram depend on type of neuronal injury.
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