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  • Title: Calcium channel agonist, (+/-)-Bay K8644, causes an immediate increase in the striatal 1-methyl-4-phenylpyridinium level following systemic administration of the dopaminergic neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, in Balb/c mice.
    Author: Samantaray S, Mohanakumar KP.
    Journal: Neurosci Lett; 2003 Jul 31; 346(1-2):69-72. PubMed ID: 12850550.
    Abstract:
    In vivo formation of 1-methyl-4-phenylpyridinium ion (MPP(+)) in the striatum, and dopaminergic neurotoxicity following systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the presence and absence of calcium channel agonist (+/-)-Bay K8644 were analyzed in Balb/c mice. We used HPLC-photodiode array detection, HPLC-electrochemical detection and spectrofluorimetric procedures to measure striatal MPP(+) and dopamine (DA) and for the assay of monoamine oxidase-B (MAO-B) activity, respectively. Systemic administration of (+/-)-Bay K8644 resulted in a significant increase in striatal MAO-B activity. An MPTP-induced decrease in striatal MAO-B activity was attenuated by pre-treatment with (+/-)-Bay K8644 initially, but not on the 3rd day. MPP(+) formation in the striatum following systemic administration of MPTP was significantly increased by the pre-treatment of the agonist initially (30 min), but was not different afterwards (at 60 and 90 min). Nevertheless, the total MPP(+) formed over a 90 min period was found to be comparable. (+/-)-Bay K8644 administration prior to MPTP failed to influence the MPTP-induced striatal DA depletion on the 3rd day. While the transient effect of (+/-)-Bay K8644 on striatal MAO-B is reflected as an immediate increase in the levels of MPP(+) in the striatum, it failed to affect MPTP-induced DA neurotoxicity in Balb/c mice.
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