Effects of d-methamphetamine on monkey brain monoamine oxidase, in vivo and in vitro.

Egashira, Toru; Yamamoto, Toshinori; Yamanaka, Yasumitsu

doi:10.1254/jjp.45.79

Cited by 14 publications

(6 citation statements)

References 26 publications

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“…The selective increase in cysteinyl-DA suggests that the oxidation occurred in a compartment in which DA exists in higher concentrations than DOPAC, such as the cytoplasm of a DA terminal. Presumably, the intracellular concentration of DA is increased after METH administration by the vesicular release of DA into the cytoplasm (Cubells et al, 1994), and cytoplasmic DOPAC levels are decreased by inhibition of monoamine oxidase by metabolites of METH (Egashira et al, 1987). Therefore, the selective increase in cysteinyl-DA suggests that the oxidation of DA occurs in the intracellular compartment.…”

Section: Discussionmentioning

confidence: 99%

Dopamine Quinone Formation and Protein Modification Associated with the Striatal Neurotoxicity of Methamphetamine: Evidence against a Role for Extracellular Dopamine

1999

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Methamphetamine-induced toxicity has been shown to require striatal dopamine and to involve mechanisms associated with oxidative stress. Dopamine is a reactive molecule that can oxidize to form free radicals and reactive quinones. Although this has been suggested to contribute to the mechanism of toxicity, the oxidation of dopamine has never been directly measured after methamphetamine exposure. In this study we sought to determine whether methamphetamine-induced toxicity is associated with the oxidation of dopamine by measuring the binding of dopamine quinones to cysteinyl residues on protein. We observed that administration of neurotoxic doses of methamphetamine to rats resulted in a two- to threefold increase in protein cysteinyl-dopamine in the striatum 2, 4, and 8 hr after treatment. When methamphetamine was administered at an ambient temperature of 5 degreesC, no increase in dopamine oxidation products was observed, and toxicity was prevented. Furthermore, as shown by striatal microdialysis, animals treated with methamphetamine at 5 degreesC showed DA release identical to that of animals treated at room temperature. These data suggest that the toxicity of methamphetamine and the associated increase in dopamine oxidation are not exclusively the result of increases in extracellular dopamine. Because dopamine-induced modifications of protein structure and function may result in cellular toxicity, it is likely that dopamine oxidation contributes to methamphetamine-induced toxicity to dopamine terminals, adding support to the role of dopamine and the evidence of oxidative stress in this lesion model.

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Section: Discussionmentioning

confidence: 99%

Dopamine Quinone Formation and Protein Modification Associated with the Striatal Neurotoxicity of Methamphetamine: Evidence against a Role for Extracellular Dopamine

1999

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“…3 and Table 1). This might be explained by the combined inhibitory effect of clorgyline and METH on MAO activity, since amphetamines inhibit MAO [30][31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine Reward in Mice as Assessed by Conditioned Place Preference Test with Supermex® Sensors: Effect of Subchronic Clorgyline Pretreatment

Kitanaka

Tatsuta

et al. 2006

Neurochem Res

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Recent studies in our laboratory have shown that methamphetamine (METH)-induced hyperlocomotion and behavioral sensitization in mice were inhibited by clorgyline, an irreversible monoamine oxidase inhibitor. In this study, the effect of clorgyline pretreatment on METH-induced rewarding effect was assessed by a conditioned place preference (CPP) test, using an apparatus developed with Supermex sensors (infrared pyroelectric sensors). Although intact male ICR mice showed significant CPP for METH (0.5 mg/kg, i.p.), pretreatment with subchronic clorgyline (0.1 and 10 mg/kg, s.c.) did not affect the magnitude of CPP. At a dose of 1 mg/kg, pretreatment of the mice with clorgyline showed a similar CPP index in both saline/saline and METH/saline pairing groups. During the conditioning session, the mice did not express behavioral sensitization to METH. Pretreatment with clorgyline (0.1, 1, and 10 mg/kg) decreased striatal apparent monoamine turnover in a dose-dependent manner. These results indicated that clorgyline pretreatment (0.1 and 10 mg/kg) did not influence the METH-induced rewarding effect in mice, although pretreatment of the mice with clorgyline at a dose of 1 mg/kg appeared to influence the CPP for METH.

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“…In order to achieve MAO-A inhibition over 200 times more selegiline is needed (7). The D-(+)-forms of amphetamines have also been shown to have MAO-A inhibitory properties (44)(45)(46). Furthermore, the levoamphetamines are three to four times weaker central stimulants than the dextro-(+)-forms (47), which in low doses release dopamine and noradrenaline from neurons containing these catecholamines.…”

Section: Discussionmentioning

confidence: 99%

Pharmacokinetics and metabolism of selegiline

Heinonen

Myllylä

Sotaniemi

et al. 1989

Acta Neurologica Scandinavica

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Abstract– Selegiline is readily absorbed from the gastrointestinal tract. It is distributed rapidly into the tissues, including the brain. It is the L‐form of selegiline that is an active MAO‐B inhibitor, the D‐(+)‐form being 25 times less active. Selegiline is metabolised into L‐(−)‐desmethylselegiline (DES), L‐(−)‐amphetamine (A) and L‐(−)‐methamphetamine (MA), mainly in the liver. We measured the steady state concentrations of the metabolites in the serum and cerebrospinal fluid (CSF) of patients with Parkinson's or Alzheimer's diseases who were on continuous selegiline therapy. The mean concentrations in serum and CSF were similar, and were not affected by the addition of levodopa. The mean concentrations of patients with Alzheimer's or Parkinson's disease were 6.5±2.5 ng/ml for A, 14.7±6.5 ng/ml for MA and 0.9±0.7 ng/ml for DES. The metabolites of selegiline were excreted in urine, and the recovery as metabolites was 87%. Due to the stereospecificity and the low CSF concentrations of the (−)amphetamine metabolites during the therapy with 10 mg selegiline, these metabolites do not seem to contribute significantly to the clinical efficacy of selegiline.

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Effects of d-methamphetamine on monkey brain monoamine oxidase, in vivo and in vitro.

Cited by 14 publications

References 26 publications

Dopamine Quinone Formation and Protein Modification Associated with the Striatal Neurotoxicity of Methamphetamine: Evidence against a Role for Extracellular Dopamine

Dopamine Quinone Formation and Protein Modification Associated with the Striatal Neurotoxicity of Methamphetamine: Evidence against a Role for Extracellular Dopamine

Methamphetamine Reward in Mice as Assessed by Conditioned Place Preference Test with Supermex® Sensors: Effect of Subchronic Clorgyline Pretreatment

Pharmacokinetics and metabolism of selegiline

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