Abstract:
:Selective loss of central dopaminergic neurons in vitro and in vivo can be initiated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) through its metabolite phenylpyridium ion (MPP+). Such MPTP-mediated cytotoxicity can be blocked by (-)-Deprenyl, a monoamine oxidase (MAO)-B inhibitor, but the exact mechanisms of MPP(+)-induced cytotoxicity and (-)-Deprenyl's protection against such neurotoxicity are not fully understood. Using a hybrid clone MES 23.5, a dopaminergic cell line that does not contain MAO-B, we document that MPP+ induces apoptotic cell death. Application of (-)-Deprenyl at concentrations of 0.1-10 microM significantly reduces MPP(+)-induced apoptosis in MES 23.5 cells; (-)-Deprenyl at higher concentrations (> 100 microM) that completely inhibit MAO-B activity, however, induces apoptosis. Pretreatment with N-(2-aminoethyl)-p-chlorobenzamide (Ro 16-6491), a selective MAO-B inhibitor, does not protect MES 23.5 cells against MPP(+)-induced cell death. These results suggest that the protective action of (-)-Deprenyl against MPP+ neuro-toxicity in dopaminergic cell line may be independent of the inhibition of MAO-B.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Le W,Jankovic J,Xie W,Kong R,Appel SHdoi
10.1016/S0304-3940(97)00170-5subject
Has Abstractpub_date
1997-03-21 00:00:00pages
197-200issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(97)00170-5journal_volume
224pub_type
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