Increased brain concentration of homovanillic acid in rats treated with <i>threo</i>-3,4-dihydroxyphenylserine

Edwards, David J.; Sedlock, M.L.

doi:10.1111/j.2042-7158.1982.tb04706.x

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…Experimental studies on rats have demonstrated that the concentration of homovanillic acid (HVA) and other DA metabolites after L-DOPS increased in the whole brain (Edwards et al, 1981(Edwards et al, , 1982, while unaltered in the striatal extracellular fluid (Brannan et al, 1990). Facilitatory effects of NE neurons on DA neurons have been shown in previous reports (Corrodi et al, 1970;Pycock et al, 1975;And6n et al, 1976).…”

Section: Discussionmentioning

confidence: 83%

The effects of L-threo-3,4-dihydroxyphenylserine on the total norepinephrine and dopamine concentrations in the cerebrospinal fluid and freezing gait in parkinsonian patients

Tohgi

Abe

Takahashi

1993

J Neural Transm Gen Sect

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We studied the effects of L-threo-DOPS (L-DOPS) on the concentrations of total (conjugated and unconjugated) dopamine (DA) and norepinephrine (NE) in the cerebrospinal fluid (CSF) of parkinsonian patients with freezing phenomenon. The NE concentration increased remarkably and dose-dependently after administration of L-DOPS in both L-dopa/carbidopa-pretreated and untreated patients. The DA concentration also increased mildly but significantly in L-dopa/carbidopa-untreated patients. Freezing phenomenon improved in 6 out of 8 patients at Hoehn and Yahr's stage III, and 1 out of 5 patients at stage IV. These results indicate that L-DOPS administration increases the NE concentration dose-dependently, and is effective for freezing of gait of moderate severity.

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Section: Discussionmentioning

confidence: 83%

The effects of L-threo-3,4-dihydroxyphenylserine on the total norepinephrine and dopamine concentrations in the cerebrospinal fluid and freezing gait in parkinsonian patients

Tohgi

Abe

Takahashi

1993

J Neural Transm Gen Sect

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“…In animal experiments Bartholini etal. (1975) found increased concentrations of 5-HIAA and HVA after treatment with D-erythro-DOPS, while Edwards and Sedlock (1982) observed increased levels of HVA after L-threo-DOPS. This was explained by the decarboxylation of DOPS to NA in dopaminergic or serotonergic neurons, thereby causing release of the resident neurotransmitters and followed by an increase of their metabolites.…”

Section: Discussionmentioning

confidence: 88%

Catecholamine metabolism during additional administration of DL-threo-3,4-dihydroxyphenylserine to patients with Parkinson's Disease

Teelken

Vandenberg

Muskiet³

et al. 1989

J Neural Transm Gen Sect

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DL-threo-3,4-dihydroxyphenylserine (DL-threo-DOPS) was administered during 10 days to 4 patients with longstanding Parkinson's disease in addition to their treatment with L-3,4-dihydroxyphenyl-L-alanine (L-DOPA)-carbidopa (Sinemet). All patients tended to improve in their symptoms freezing, all day life activity and mood. There were no improvements in rigidity, tremor, and akinesia (in general). During the DL-threo-DOPS-treatment cerebrospinal fluid (CSF), serum and urine concentrations of catecholamines were measured. The results show that DL-threo-DOPS is transported to the brain and CSF in a way comparable with L-DOPA. However, no measurable increase of 3-methoxy-4-hydroxyphenylethyleneglycol (MOPEG) in CSF could be demonstrated. This suggests that the synthesis of noradrenaline from DL-threo-DOPS in the brain is doubtful. In addition measurements in urine reveals that at the dose used Sinemet prevents peripheral decarboxylation of DL-threo-DOPS into noradrenaline. Other possible metabolic pathways of DL-threo-DOPS are discussed.

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“…The action of L-threo-DOPS in the treatment of parkinsonism is now considered to be due to the increase in NE concentration in the brain (Narabayashi et al, 1981), which is caused by the enzymic decarboxylation of L-DOPS incorporated into the brain (Nakamura et al, 1985). However, the transport of L-threo-DOPS through the bloodbrain barrier into the brain is limited (Edwards and Sedlock, 1982) and a marked increase in NE level in the brain cannot be expected. Another explanation of the mechanism of L-threo-DOPS is that L- (Tanaka et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Monoamine Oxidase by 3,4‐Dihydroxyphenylserine

Naoi

Nagatsu

1986

Journal of Neurochemistry

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The effects of diastereomers of 3,4-dihydroxyphenylserine (DOPS) on the enzyme activity of rnonoamine oxidase (MAO) in human placenta and liver mitochondria were examined. Both L-and D-threo-DOPS were found to inhibit MAO-A in human placental mitochondria in competition with the substrate, and the K , values for L-and D-threo-DOPS obtained were 68.3 and 125 p M , respectively. The inhibitory effect of L-threo-DOPS on both MAO-A and -B activity was confirmed in human liver mitochondria, and MAO-A was found to be more sensitive to the inhibitor. Other isomers of DOPS, L-and D -~Q T~~o -D O P S , were found to inhibit M A 0 ac-Abbreviations used: AADC, aromatic L-amino acid decarboxylase; DA, 3,4-dihydroxyphenylethylamine (dopamine); DOPS, 3,4-dihydroxyphenylserine; MAO, monoamine oxidase; NE, norepinephrine. -NSD-1055 NSD-1055 (100 &A4) Control 2.65 5 0.09 (100.0%) 1.63 ? 0.06 (100.0%) L-threo-DOPS (100 FM) 0.81 ? 0.03 (50.0%) D-threo-DOPS (100 CCM) 1.14 ? 0.09 (70.0%) L-eryrhro-DOPS (100 kA4) 1.90 2 0.07 (71.7%) 1.15 ? 0.06(70.7%) D-erythro-DOPS (100 ph') 1.15 ? 0.02 (70.7%) 1.31 ? 0.10 (49.4%) 1.75 5 0.03 (66.2%) 1.82 2 0.01 (68.5%) Each value is the mean S SEM of three experiments. 0 The final kynuramine concentration used was 100 )I.M.

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Increased brain concentration of homovanillic acid in rats treated with threo-3,4-dihydroxyphenylserine

Cited by 10 publications

References 8 publications

The effects of L-threo-3,4-dihydroxyphenylserine on the total norepinephrine and dopamine concentrations in the cerebrospinal fluid and freezing gait in parkinsonian patients

The effects of L-threo-3,4-dihydroxyphenylserine on the total norepinephrine and dopamine concentrations in the cerebrospinal fluid and freezing gait in parkinsonian patients

Catecholamine metabolism during additional administration of DL-threo-3,4-dihydroxyphenylserine to patients with Parkinson's Disease

Inhibition of Monoamine Oxidase by 3,4‐Dihydroxyphenylserine

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