PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Dimethoxyphenylethylamine”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1985

Projection of an endocoid involved with schizophrenic reaction.

Administration of 3,4-dimethoxyphenylethylamine, (DMPEA) which has been incubated with blood plasma from unmedicated, acute schizophrenics, to aggregated mice pretreated with the monoamine oxidase inhibitor, phenylisobutylhydrazine, has been shown to produce an amphetamine-like excitatory, lethal response in such mice. Use of blood plasma from 92 unmedicated, acute schizophrenics in the test system giving that response yielded 82 positive responses (89%) and 10 negative responses (11%). Substitution of the blood plasmas from 94 non-schizophrenics analogously into this test system produced 2 positive responses (2%) and 92 negative responses (98%). When plasma from schizophrenics medicated with antipsychotic tranquilizers were tested in the system, none gave positive response, 58 gave negative response. If the compound bis-N, N dimethoxyphenylethylamine (bis-DMPEA) was either added to DMPEA or substituted for it and incubated with inactive blood plasma taken from non-schizophrenics in the incubation step of the test system a marked positive response was elicited. The results obtained are compatible with a hypothesis which postulates function of a DMPEA metabolite as a pathologic endocoid in schizophrenic reaction.

Acute Disease↗
PubMed2004

Inhibition of brain mitochondrial respiration by dopamine and its metabolites: implications for Parkinson's disease and catecholamine-associated diseases.

A structure-potency study examining the ability of dopamine (DA), its major metabolites and related amine and acetate congeners to inhibit NADH-linked mitochondrial O(2) consumption was carried out to elucidate mechanisms by which DA could induce mitochondrial dysfunction. In the amine studies, DA was the most potent inhibitor of respiration (IC(50) 7.0 mm) compared with 3-methoxytryramine (3-MT, IC(50) 19.6 mm), 3,4-dimethoxyphenylethylamine (IC(50) 28.6 mm), tyramine (IC(50) 40.3 mm) and phenylethylamine (IC(50) 58.7 mm). Addition of monoamine oxidase (MAO) inhibitors afforded nearly complete protection against inhibition by phenylethylamine, tyramine and 3,4-dimethoxyphenylethylamine, indicating that inhibition arose from MAO-mediated pathways. In contrast, the inhibitory effects of DA and 3-MT were only partially prevented by MAO blockade, suggesting that inhibition might also arise from two-electron catechol oxidation and quinone formation by DA and one-electron oxidation of the 4-hydroxyphenyl group of 3-MT. In the phenylacetate studies, 3,4-dihydroxyphenylacetic acid (DOPAC) was equipotent with DA in inhibiting respiration (IC(50) 7.4 mm), further implicating the catechol reaction as the cause of inhibition. All other carboxylate congeners; phenylacetic acid (IC(50) 13.0 mm), 4-hydroxyphenylacetic acid (IC(50) 12.1 mm), 4-hydroxy-3-methoxyphenylacetic acid (HVA, IC(50) 12.0 mm) and 3,4-dimethoxyphenylacetic acid (IC(50) 10.2 mm), were equipotent respiratory inhibitors and two- to fourfold more potent than their corresponding amine. These latter findings suggest that the phenylacetate ion can also contribute independently to mitochondrial inhibition. In summary, mitochondrial respiration can be inhibited by DA and its metabolites by four distinct MAO-dependent and independent mechanisms.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Effects of dopamine metabolites on locomotor activities and on the binding of dopamine: relevance to the side effects of L-dopa.

L-dopa is the major treatment for Parkinson's disease (PD), but its efficacy is limited by the presence of dyskinesia. The dyskinesia develops over a period of exposure to L-dopa and is related to the dosage, therefore, the cause may involve inductive changes that produce toxic levels of metabolites, interfering with dopamine (DA) neurotransmission. Chronic L-dopa induces catechol-O-methyltransferase (COMT) and methionine adenosyl transferase (MAT), enzymes involved in the methylation of catecholamines (CA). In addition, high levels of 3-O-methyl-dopa have been reported in the plasma of dyskinetic PD patients, treated with L-dopa, as compared to non-dyskinetic patients, therefore, the methyl metabolites of CA may be increased during L-dopa therapy and may be involved in the dyskinesia. Since large amounts of DA are produced from L-dopa, and DA is extensively methylated, the methyl metabolites of DA, 3-methoxytyramine (3-MT) and 3,4-dimethoxyphenylethylamine (DIMPEA), may be also involved. The first step in knowing this, is to assess the behavioral and DA-receptor activities of 3-MT and DIMPEA. In the rat, the intraventricular injection of 0.5 micromol of DIMPEA increased the total distance traveled (TD) by over 100%, the number of movement (NM) made by 40% and the time spent moving (MT) by about 36%. Identical doses of 3-MT decreased the TD by 42%, NM by 22% and MT by 39%. DIMPEA (1 mM) increased the binding of DA with brain membranes by 44.7%, whereas 3-MT decreased it by 15.8%. The results show that 3-MT and DIMPEA are behaviorally active, and in parallel, they interact with the binding sites for DA, consequently, they may contribute to the side effects of L-dopa. L-dopa produces high levels of DA and induces MAT and COMT. It is proposed, therefore, that DA will be methylated to 3-MT and 3-MT to DIMPEA. At threshold level each product will inhibit, allosterically, its enzyme of methylation, causing sequential and rhythmic up and down regulation of its concentration. At peak levels these hydrophobic metabolites will modulate the actions of DA on synaptic membranes, causing abnormal movements, at times, resembling the "on-off effects".

Animals↗
PubMed1975

Serotoninergic control of rat growth hormone secretion.

The ability of 5-hydroxyl-L-tryptophan (5-HTP) or pentobarbital anesthesia to elevate rat serum GH levels is completely blocked by the simultaneous administration of the serotonin antagonist cyprophepatidine, as well as by the pineal gland principles melatonin and 5-methoxytryptamine (5-MT), and by the 0-methylated dopamine derivative 3,4-dimethoxyphenylethylamine (DMPEA). Small doses of 5-MT cause paradoxical elevations in serum rat GH but at the same time inhibit the action of 5-HTP. Blockade of dopaminergic pathways by treatment with either DMPEA or chlorpromazine causes a slight, nonsignificant suppression of serum GH in normal rats while serum prolactin levels are increased greater than tenfold showing that, unlike prolactin, rat GH is not subject to tonic inhibitory control by dopamine. The data presented support the recently advanced hypothesis that rat GH is under serotoninergic CONTROL AND DEMONSTRATE THAT GH secretion can be significantly suppressed by serotoninergic blockade. It is suggested that the results presented here for monoamine control of rat GH release are not a variance with those reported for man.

5-Methoxytryptamine↗
PubMed1976

Biogenic amine control of growth hormone secretion in the fetal and neonatal rat.

The development of the hypothalamic-pituitary axis for growth hormone (GH) secretion has been studied in the rat fetus and in the neonate 4, 24, 48 and 72 h after birth. Injections of the serotonin blocker cyproheptadine (Cypro) and a catecholamine, dopamine (DA), each led to reductions in the level of serum GH in 21 to 22 day fetuses and in neonates up to 3 days after birth. The O-methylated derivative of dopamine, dimethoxyphenylethylamine (DMPEA), did not alter serum GH levels from those seen in saline-treated control animals. These results indicate that biogenic amines exert control over GH secretion in the fetus, close to term, and in early neonatal period. They suggest that this control is similar to that seen in the adult rat and in man and that such control may operate through serotonin receptors.

Animals↗
PubMedDate not supplied

[DNA fusion in the presence of catecholamines and substances close to them in structure].

Using an Cphi-4A spectrophotometer (USSR), denaturation of DNA containing approximately 2% residual protein has been studied in the presence of catecholamines and their precursors: epinephrine, beta-3,4-dioxyphenylalanine, norepinephrine, 3,4-dimethoxyphenylethylamine, tyrosine, and phenylalanine. All these substances, excluding phenylalanine, induce positive excessive hyperchromicity (as compared to initial DNA). The correlation between this effect and molecular structures of the substances studied has been shown to exist. An increase of DNA hyperchromicity in the presence of catecholamines has been found to result from the oxygen presence in the aromatic rings of the catecholamines molecules. It is assumed that the interaction between the negative O-atoms in catecholamines and bivalent metal cations in the nucleoprotein complex weakens the DNA-protein binding. This leads to an additional disorientation due to the heat of nucleic acid bases, which were previously bound by the residual protein.

Catecholamines↗