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At least 19 recordsLinked to original sources
PubMed1996

Effect of dopamine, dimethoxyphenylethylamine, papaverine, and related compounds on mitochondrial respiration and complex I activity.

We report the effect of papaverine, tetrahydro-papaverine, laudanosine, dimethoxyphenylethylamine, dopamine, and its metabolites on mitochondrial respiration and activities of the enzymes in the electron transfer complexes, as mitochondrial toxins may be implicated in the etiology and the pathogenesis of Parkinson's disease. Papaverine was the most potent inhibitor of complex I and NADH-linked mitochondrial respiration among the compounds tested next to rotenone. Tetrahydropapaverine, dimethoxyphenylethylamine, and laudanosine also inhibited NADH-linked mitochondrial respiration and complex I activity in this order. Dopamine and its metabolites showed either no inhibition or only very week inhibition. Compounds with dimethoxy residues in the phenyl ring were associated with more potent inhibition of complex I than those without. Our results warrant further studies on these and some related compounds as candidate neurotoxins causing Parkinson's disease.

Animals↗
PubMed1977

Facilitation and disruption by mescaline and 3,4-dimethoxyphenylethylamine of shock avoidance in rats.

The effects of mescaline hydrochloride (4.95-79.2 mg/kg i.p.) and its non-hallucinogenic analogue 3,4-dimethoxyphenylethylamine hydrochloride (DMPEA) (12.5-100 mg/kg i.p.) on shock avoidance in a shuttlebox were studied in male Long-Evans rats trained to high (above 88%, good performers) or low (below 6%, poor performers) stable base-line avoidance rates. In good performers, mescaline and DMPEA caused a dose-dependent decrease in avoidance rate (ED 50's 44.6 and 39.2 mg/kg, respectively) without affecting presession (5-min adaptation period) or intertrial shuttlebox crossings. In poor performers, mescaline caused a dose-dependent increase in avoidance rate (ED 50 = 24.8 mg/kg) and intertrial crossings, without affecting presession crossings. The results suggest that mescaline, but not DMPEA, has dual facilitative and disruptive effects on avoidance behavior at similar dose ranges. The facilitative, but not the disruptive, effect may be related to changes in motor activity.

Animals↗
PubMed1978

Methodical investigation of the production of antibodies towards 3,4-dimethoxyphenylethylamine.

In this study the synthesis of various antigens from 3,4-dimethoxyphenylethylamine (3,4-DMPEA) is described. Antigen A was formed by coupling the acylated side chain of 3,4-DMPEA to the protein, while antigen B was synthesized by introducing an acylated amino group to the benzene ring and linking this reactive group to the protein. With antigen A an antiserum with a titer of 1 : 16000 could be raised, while with antigen B coupled to human albumin and bovine gamma-globulin the antiserum had a titer of 1 :1000 and 1 : 4000. Antibodies formed by immunization with antigen A exhibited a high specificity for substituents of the benzene ring, but were less specific for substituents of the side chain. Antibodies formed by treatment with the antigen B were specific for both kinds of substituents. So far, it has not been possible to harvest any specific antibodies towards the corresponding antigens of dopamine.

Animals↗
PubMed1978

3,4-Dimethoxyphenylethylamine excretion of normals and schizophrenics, behaviour during total fasting.

A specific and sensitive radioimmunoassay for the determination of 3,4-dimethoxyphenylethylamine (3,4-DMPEA) in urine was developed. In 5 fasting healthy volunteers excretion of 3,4-DMPEA was not diminished, indicating that this substance can be regarded as an endogenous metabolite. In addition, the time profile of the excretion of 3,4-DMPEA was measured in one patient during total fasting. In 25 patients with schizophrenic psychoses, 9 psychiatric patients without schizophrenia and 80 control patients excretion of 3,4-DMPEA was compared. No significant differences could be observed between these three groups.

Adult↗
PubMed1997

Neurotoxic effects of papaverine, tetrahydropapaverine and dimethoxyphenylethylamine on dopaminergic neurons in ventral mesencephalic-striatal co-culture.

We report neurotoxic effects of papaverine, tetrahydropapaverine, dimethoxyphenylethylamine (DMPEA), and 1-methyl-4-phenylpyridinium ion (MPP+) on dopaminergic neurons in ventral mesencephalic-striatal co-culture. These compounds have been reported as mitochondrial toxins which may be implicated in the etiology and pathogenesis of Parkinson's disease. Tyrosine hydroxylase (TH)-positive neurons were decreased in dose-dependent manner by these compounds. Papaverine and MPP+ were most toxic to TH-positive neurons among the compounds tested. The order of the toxicity on TH-positive neurons was papaverine, MPP+, tetrahydropapaverine and then DMPEA. This order of toxicity was approximately the same as that reported on the inhibitory effect of these compounds on NADH-linked mitochondrial respiration and complex I activity. These findings indicate that the presence of dimethoxy residues in the catechol ring augments toxicity to dopaminergic neurons in culture.

1-Methyl-4-phenylpyridinium↗
PubMed1997

Dimethoxyphenylethylamine and tetrahydropapaverine are toxic to the nigrostriatal system.

We report the toxic effects of 3,4-dimethoxyphenylethylamine (DMPEA), and tetrahydropapaverine (THP) on the rat nigrostriatal system; THP is a tetrahydroisoquinoline compound which may be derived from DMPEA by conjugation of DMPEA and its oxidative metabolite, dimethoxyphenylacetaldehyde; both are potent inhibitors of mitochondrial complex I. These compounds were introduced to the unilateral caudate-putamen of male Sprague-Dawley rats over 7 days using a 200-microl mini-osmotic pump. Striatal dopamine on the injected side showed a significant decrease to 86% of the non-injected side after 16.55 micromol/7 days infusion of DMPEA, and to 73% of the non-injected side after 7.90 micromol/7 days of THP infusion; as the non-injected side dopamine also reduced in the THP-injected rats, dopamine on the injected side was 55% of the saline control. Tyrosine hydroxylase (TH)-positive nigral neurons were decreased to 76% of the non-injected side after 16.55 micromol/7 days infusion of DMPEA and to 77% after 7.90 micromol/7 days of THP infusion. Dimethoxyphenyl-tetrahydroisoquinoline compounds appear to be potent nigral neurotoxins.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Uptake of 3,4-dimethoxyphenylethylamine-1-14C (14C-DMPEA) by rat tissues in vitro.

Rat heart and spleen slices were incubated with 3,4-dimethoxyphenylethylamine-1-14C(14C-DMPEA) in Krebs medium at 37 C. At the end of 5-20 min of incubation, the heart did not take up the radioactivity while the spleen did. The Km and Vmax values of uptake in the spleen were 1 x 10(-4) M and 20 nmole/g per min, respectively, and the uptake was reduced to 16.0-35.1% in the cold (4 C) and to 40.3-64.0% in Na+-free medium. Thus, the uptake was an energy-dependent active process but was only partially Na+-dependent. Spleen slices incubated with 14C-DMPEA-free medium for 15 min following incubation with 14C-DMPEA retained 41.0-74.8% of radioactivity. The uptake was insensitive to norepinephrine (0.313 and 0.939 muM), dopamine (9.98 muM), 5-hydroxytryptamine (5 muM), cocaine (14.8 muM), 1-amphetamine (0.3 and 300 muM), d-amphetamine (300 muM), and normetanephrine (45.7 muM). 6-Hydroxydopamine treatment of rats, which produced 93% reduction in the splenic norepinephrine content, did not significantly reduce uptake. Thus, the uptake of DMPEA into the spleen is not by adrenergic neurones.

Amphetamine↗
PubMed1975

Comparison of 3,4-dimethoxyphenylethylamine treated plasma from chronic schizophrenics and controls.

Plasma samples were collected from chronic schizophrenic patients not on drug therapy and from non-psychotic hospital volunteet controls and incubated with 3,4-dimethoxywhenylethylamine (DMPEA) when injected into monoamine oxidase inhibitor (MAOI) pretreated mice who were then aggregated (groups of 5 ea.) for four hours, the two kinds of plasma produced results so similar that no differences between them could be observed. Doubling the amount of plasma and DMPEA likewise failed to differentiate plasma origin. In our hands no differentiation between plasma samples from control subjects and schizophrenic patients could be determined under the conditions employed.

Amphetamine↗