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  • 1
    Electronic Resource
    Electronic Resource
    Intracerebroventricular Administration of l-Buthionine Sulfoximine: A Method for Depleting Brain Glutathione (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Sprague-Dawley rats (200-260 g) were anesthetized with chJoral hydrate (400 mg/kg) and polyethylene cannulae were permanently implanted into the lateral ventricles. One or two days later, l-buthionine-[S,R]-sulfoximine (L-BSO), an apparently selective inhibitor of γ-glutamylcysteine synthetase, was administered intracerebroventricularly through the cannulae. The brain content of glutathione (GSH) was determined by HPLC with electrochemical detection (gold/ mercury electrode) using N-acetylcysteine as internal standard. A time-course study of the changes in the striatum following a single dose of l-BSO (3.2 mg) revealed a maximal depletion of GSH (-60%) approximately 48 h after the administration. The effects of various doses of l-BSO on GSH in the striatum, in the limbic region, and in the cortex were assessed at 24 h and 48 h after the administration. l-BSO (0.02-3.2 mg) produced dose-dependent reductions of GSH in all brain regions studied at both time intervals. In a long-term experiment l-BSO (3.2 mg) was administered every second day. After 4 days, i.e., after two injections, striatal GSH was reduced by approximately 70%. No further depletion of GSH was obtained by additional injections of l-BSO, but GSH was maintained at this low level for the 12 days studied. These results suggest that l-BSO, administered intracerebroventricularly, would serve as a useful tool for evaluation of the biological role of GSH in the CNS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09256.x
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  • 2
    Electronic Resource
    Electronic Resource
    In Vivo Autoxidation of Dopamine in Guinea Pig Striatum Increases with Age (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Catechols are known to react readily with molecular oxygen to form the corresponding quinones together with reduced oxygen species. These products have been shown to be toxic in in vivo and in vitro systems. 5-S-Cysteinyl adducts of catechols are believed to be formed through the spontaneous reaction between quinones and thiol-containing compounds, like cysteine and glutathione (GSH). Thus, the brain levels of these adducts probably indicate the autoxidation rate of catechols in vivo. In the present study, the striatal concentrations of 5-S-cysteinyldopamine (5-S-cysteinyl-DA), 5-S-cysteinyl-3,4-dihydroxyphenylalanine (5-S-cysteinyl-DOPA), and 5-S-cysteinyl-3,4-dihydroxyphenylacetic acid (5-S-cysteinyl-DOPAC) were determined in 2-week-, 2-month-and 3-year-old guinea pigs. In addition, brain levels of DA, the DA metabolite DOPAC, and GSH were assessed. The concentration of 5-S-cysteinyl-DA increased markedly with age. The 3-year-old guinea pigs had the highest level, i.e., 248% of the concentration in the 2-week-old animals and 219% of the concentration in the 2-month-old animals. Furthermore, the striatal 5-S-cysteinyl-DOPA level in the 3-year-old group was 68% higher than in the 2-week-old group and 46% higher than in the 2-month-old group. No age difference in the striatal concentration of DA was found. In contrast, the concentration of DOPAC increased with age: The DOPAC level in the 3-year-old animals was 153% of the level in the 2-week-old animals and 116% of the level in the 2-month-old animals. A slight decrease in brain GSH content was observed between 2 weeks and 2 months, whereas the level in the 3-year-old animals was not significantly different from the concentration in the 2-month-old animals. Thus, the present study has shown an increase in 5-S-cysteinyl-DA and 5-S-cysteinyl-DOPA levels with age in guinea pig striatum. The rise in 5-S-cysteinyl-DA content was larger than the increase in content of the DA metabolite DOPAC, a finding indicating that DA to a greater extent undergoes autoxidation with increasing age. This may be part of the mechanism underlying the loss of dopaminergic neurons in senescence and in Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04183.x
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  • 3
    Electronic Resource
    Electronic Resource
    Reduction of Brain Glutathione by l-Buthionine Sulfoximine Potentiates the Dopamine-Depleting Action of 6-Hydroxydopamine in Rat Striatum (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Sprague-Dawley rats were anesthetized with chloral hydrate, and plastic cannulae were permanently implanted into the lateral ventricles. The animals then were allowed to recover for 1–2 days. L-Buthionine sulfoximine (l-BSO), a selective inhibitor of glutathione (GSH) synthesis, and 6-hydroxydopamine (6-OH-DA), a selective catecholaminergic neurotoxin, were administered intracerebroventricularly. The striatal concentrations of GSH and monoamines were determined by HPLC with electrochemical detection. Two injections of l-BSO (3.2 mg, at a 48-h interval) resulted in a 70% reduction of striatal GSH. 6-OH-DA (150 or 300 μg) reduced the concentrations of striatal dopamine and noradrenaline 7 days after the administration, but left the concentrations of 5-hydroxytryptamine unaltered. L-BSO treatment did not produce any changes in the levels of monoamines per se but it potentiated the catecholamine-depleting effect of 6-OH-DA in the striatum. Thus, GSH appears to suppress the toxicity of 6-OH-DA, probably by scavenging the toxic species formed during 6-OH-DA oxidation. In view of these results one may suggest an important role for GSH in catecholaminergic neurons: protecting against the oxidation of endogenous catechols.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb02550.x
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  • 4
    Electronic Resource
    Electronic Resource
    3-Methoxytyramine Formation Following Monoamine Oxidase Inhibition Is a Poor Index of Dendritic Dopamine Release in the Substantia Nigra (1997)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 69 (1997), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: This study was undertaken, using microdialysis, to compare the extracellular concentration of 3-methoxytyramine and dopamine in dialysate from the striatum and substantia nigra, after pargyline (75 mg/kg), after pargyline plus amphetamine (3 mg/kg), and after pargyline plus reserpine (5 mg/kg) administration. Treatment with pargyline alone increased the extracellular dopamine concentration by 70% in the striatum and by 140% in the substantia nigra and induced in both regions a time-dependent accumulation of 3-methoxytyramine. The addition of d-amphetamine to pargyline increased the extracellular dopamine concentration, compared with pargyline-treated controls, to the same extent in both the substantia nigra (maximally by 360%) and the striatum (maximally by 400%), but the concomitant increase of 3-methoxytyramine accumulation in the dialysate was relatively smaller in the substantia nigra compared with the striatum. Reserpine treatment decreased the extracellular dopamine concentration in both regions below the detection level (〈10% of basal value). When pargyline was added to reserpine, the striatal extracellular dopamine concentration increased to 50% of pargyline-treated controls and the striatal 3-methoxytyramine accumulation was less than in pargyline-treated controls. However, in the substantia nigra, the addition of pargyline to reserpine resulted in dopamine concentrations as high as after pargyline only and the 3-methoxytyramine accumulation was not changed compared with pargyline-treated controls. In summary, our results indicate that dopamine in the substantia nigra is released from reserpine-sensitive storage sites and that pargyline-induced 3-methoxytyramine accumulation is a poor indicator of the local dopamine release. The latter observation may be explained by the fact that the dopamine-metabolizing enzyme, catechol-O-methyltransferase, is located inter alia in the dopamine-containing cell bodies/dendrites in the substantia nigra, in contrast to the situation in the terminals in the striatum where catechol-O-methyltransferase is located only in nondopaminergic cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1997.69041684.x
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  • 5
    Electronic Resource
    Electronic Resource
    An electrophysiological analysis of the actions of the 3-PPP enantiomers on the nigrostriatal dopamine system (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 329 (1985), S. 344-354 
    Details
    ISSN: 1432-1912
    Keywords: 3-PPP enantiomers ; Dopamine agonists ; Dopamine receptors ; Single unit recording ; Micro-iontophoresis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular single unit recording and micro-iontophoretic studies were carried out in chloral hydrate-anesthetized and gallamine-paralyzed rats to investigate the actions of the enantiomers of the dopamine (DA) analogue 3-(3-hydroxyphenyl)-N-n-propylpiperidine, 3-PPP, on the nigrostriatal DA system. Intravenously administered (+)-or (−)-3-PPP consistently inhibited nigral DA neuronal activity; these actions were readily antagonized by haloperidol but were not affected by a pretreatment of reserpine plus alpha-methyltyrosine. In contrast to (+)-3-PPP, the (−)-enantiomer produced only partial inhibition of the majority of cells studied and was also capable of partially reversing the inhibitory action of apomorphine. A prior hemitransection of the brain did not alter the inhibitory action of either enantiomer. Whereas iontophoretically ejected (+)-3-PPP consistently reduced DA cell firing rate, similarly applied (−)-3-PPP reduced the activity of only some DA cells, while the majority were not influenced. In addition, iontophoresis of (−)-3-PPP could reduce the inhibitory effect of similarly applied DA or (+)-3-PPP. The (+)-enantiomer reduced caudate neuronal activity both after intravenous administration and iontophoresis. Intravenously administered (−)-3-PPP failed to influence or increased the activity of these neurons and reversed the inhibitory action of apomorphine. However, iontophoretically ejected drug reduced caudate cell activity and did not influence the inhibitory action of DA. The activity of non-DA zona reticulata neurons was inconsistently influenced by the 3-PPP enantiomers. It is concluded that (+)-3-PPP is a directly acting DA agonist, stimulating both DA autoreceptors and postsynaptic DA receptors. In contrast, (−)-3-PPP appears to be a partial agonist at nigral DA autoreceptors, whereas the action of the drug at putative postsynaptic DA receptors in the caudate remains to clarified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00496366
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  • 6
    Electronic Resource
    Electronic Resource
    GBR 13098, a selective dopamine uptake inhibitor; behavioural, biochemical and electrophysiological studies (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 383-387 
    Details
    ISSN: 1432-1912
    Keywords: GBR 13098 ; Dopamine uptake inhibition ; Locomotor activity ; Dopamine synthesis ; Neuronal activity ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous in vitro studies have suggested that GBR 13098 (1-(2-(bis(4-fluophenyl methoxy) ethyl)-4-(3-(4-fluorophenyl)-propyl)piperazine) dimethane sulfonate) acts as a selective dopamine uptake inhibitor. In the present study, behavioural, biochemical and electrophysiological effects of GBR 13098 in rats were analyzed. GBR 13098 (10–40 mg/kg, i.p.) increased locomotor activity of habituated rats. The effect was almost totally prevented by pretreatment with the monoamine-depleting drug reserpine (5 mg/kg, 6 h) or the dopamine receptor antagonist haloperidol (0.3 mg/kg, 30 min). GBR 13098 (20 mg/kg, i.p.) reduced DOPA formation in the striatum and in the limbic region, whereas the dopamine poor hemispheres were unaffected in this regard. GBR 13098 (0.1–20 mg/kg, i.v.; or 20 mg/kg, i.p.) did not alter the spontaneous firing rate of dopamine neurons in the substantia nigra zona compacta. However, pretreatment with the drug (20 mg/kg, i.p., 10–30 min) enhanced the inhibitory response of microiontophoretically applied dopamine onto the dopamine neurons of substantia nigra. Taken together, the present series of experiments show that GBR 13098 acts as a specific and potent inhibitor of dopamine uptake in brain. Present electrophysiological data are in line with the existence of a somatic or dendritic uptake system of dopamine within the substantia nigra but do not support the notion that the impulse activity of nigral dopamine neurons is regulated via a striatonigral feedback pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569374
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