Rat brain-uptake index for phenylethylamine and various monomethylated derivatives.

Phenylethylamine and its monomethylated derivatives p-methylphenylethylamine, α-methylphenylethylamine, phenylethylamine itself, N-methylphenylethylamine, o-methylphenylethylamine, and β-methylphenylethylamine, readily cross the blood-brain barrier showing a brain-uptake index (%) ± SD (water considered 100 %), of 108 ± 11, 98 ± 14, 83 ± 6, 78 ± 11, 62 ± 7 and 56 ± 6, respectively (injection of tritiated water and 100 μg standard amine, which was measured by gas-liquid chromatography). Similar brain-uptake index values (determined by double isotope counting) were obtained for phenylethylamine and α-methylphenylethylamine (amphetamine) after the injection of tritiated water and C(14)-labeled amine (either 3 μg or when added 100 μg standard compound), suggesting that they entered the brain via passive diffusion. Accordingly, both amines distributed rather evenly in the various rat brain areas examined: uptake index (%) ± SD (double isotope counting; non-, and diluted labeled amine) for phenylethylamine (89 ± 8 and 78 ± 7, 83 ± 9 and 86 ± 9, 96 ± 6 and 84 ± 7) and for α-methylphenylethylamine (88 ± 11 and 87 ± 9, 93 ± 14 and 87 ± 11, 97 ± 12 and 87 ± 9) for the cerebellum, frontal cortex, and striatum, respectively.

Changes in plasma methionine-enkephalin levels associated with a cluster headache episode.

Eighteen male cluster headache (CH) inpatients within a CH series participated in this research. Blood samples were drawn from patients at least 6-hour pain-free after the last acute CH episode and then shortly prior (SP), during, and soon after (SA) a new acute CH attack. Three healthy male, age-comparable drug-free volunteers served as controls; 5 samples were obtained from each of these individual over a 24-hour period.

Hydroxylation of phenylethylamine by rat liver preparations. Inhibition studies.

1. Rat liver 100,000 g pellet microsomal fraction p-hydroxylate phenylethylamine to tyramine in a relatively slow proceeding, NADPH-requiring reaction; Km 2.1 x 10(-5) M and Vmax 0.

Studies of the in vitro human plasma degradation of methionine-enkephalin.

1. Incubation of [3H]tyrosine methionine-enkephalin (6 x 10(-9) M final concentration) with human platelet-poor plasma (1:9 ratio to Trizma Base buffer, pH 7.4) results mostly (greater than 95%) in hydrolysis of the tyrosyl-glycine peptide bond.

Phenylethylamine metabolism to tyramine by postmortem human brain preparations.

Human brain preparations obtained from either the putamen, thalamus, hippocampus or lateral occipital gyrus p-hydroxylate phenylethylamine to tyramine, a reaction carried out by a microsomal (100,000 xg pellet) membrane bound, NADPH-requiring enzyme. This is a minor metabolic pathway occurring in chronic psychiatric patients, as well as in age-comparable controls.

Nasogastric compared with nasoduodenal feeding in low birthweight infants.

One hundred successive infants weighing less than 1500 g at birth were allocated alternately to intermittent nasogastric or continuous nasoduodenal feeding regimens. Eighty were appropriate for gestational age, and of these 25 fed successfully by nasogastric tube and 16 tolerated nasoduodenal feeding until 1600 g. No significant differences in either calorie intake or growth rates were identified throughout the seven weeks of the study.

Platelet monoamine oxidase activity and plasma levels of non-catecholic phenylethylamines in insulin-dependent diabetic subjects.

The activity of blood platelets monoamine oxidase (MAO) was significantly reduced in a group of insulin-dependent diabetics when compared to sex- and age-matched controls. This enzymatic change was accompanied by a dramatic increase in the plasma levels of phenylethylamine, whereas no significant changes were observed for the concentration of either p-tyramine or phenylethanolamine. Levels of the o- and m-isomers of tyramine were below detectable limits (less than 0.

Water pollution and diseases in fish (an epizootiologic survey).

Three watersheds, varying from highly polluted or moderately polluted to essentially pollution-free, were surveyed to determine the frequency of fish disease. Over a five year period, it was found that a relationship existed between the level of pollution and frequency of disease. The occurrence rates of microbial and oncogenic diseases increased similarly in relation to increases in pollution in the waters.

Effects of monoamine oxidase inhibitors on the borohydride stabilizable binding of serotonin and tryptamine in brain.

The in vivo and in vitro effects of various monoamine oxidase inhibitors (MAOI) on the borohydride stabilizable finding of serotonin (5-HT) or tryptamine in brain was investigated. A significant correlation between the extent of Mao inhibition and the amount of stabilized binding of the indolealkylamines was demonstrated. All hydrazine-type MAOI and harmine, a reversible nonhydrazine-type MAOI, employed in vitro, were shown to decrease the binding.

Studies on membrane receptor sites for serotonin in the brain.

The competitive effect of 5,6-dihydroxytryptamine, morphine and chlorpromazine on the binding of serotonin (5-HT) to rat brain slices was investigated. Ths busynaptosomal localization of the binding of morphine in bovine midbrain preparations was compared to that of 5-HT and found to be considerably higher. The condensation of 5-HT and tryptamine receptor carbonyl groups in brain with phenylisopropylhydrazine was shown in vitro and vivo.

Subsynaptosomal localization and biochemical characterization of serotonin binding sites in the brain.

The subsynaptosomal distribution of the borohydride stabilizable binding of serotonin (5-HT) in the brain was investigated using various enzyme markers, such as NAD glycohydrolase (NADase), Na+, K+-activated ATPase for synaptic membranes, and monoamine oxidase (MAO) for outer mitochondrial membranes. The gross distribution of the activity of NADase and Na+, K+-activated ATPase in various membrane fractions was found to parallel the distribution of 5-HT binding in these fractions. Radioactivity bound to brain fractions was extractable with chloroform-methanol (2:1).