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At least 1,441 records · Page 80Linked to original sources
PubMed1983

Storage of biogenic amines in guinea-pig brain synaptosomes: influence of proton gradient and membrane potential.

1 The effects of K(+), NaCN and the ionophores monensin, nonactin and carbonyl-cyanide-p-trifluoro-methoxyphenylhydrazone (FCCP) on the contents of [(3)H]-5-hydroxytryptamine ([(3)H]-5-HT), [(3)H]-dopamine and [(3)H]-noradrenaline ([(3)H]-NA) in guinea-pig synaptosomes preloaded with these amines were measured.2 In the presence of Ca(2+), K(+) markedly reduced the amine content of the synaptosomes, indicating an acceleration of spontaneous amine release. In the absence of Ca(2+), K(+) had much less effect.3 Monensin, nonactin and FCCP caused a release of all the three labelled amines. This release was considerably faster and more marked than that induced by K(+) and showed no dependence on Ca(2+). The ionophores did not release lactate-dehydrogenase from synaptosomes.4 NaCN, a blocker of oxidative energy production, did not enhance the spontaneous release of [(3)H]-5-HT nor did it influence the monensin-induced release of [(3)H]-5-HT.5 It is concluded that (a) the intragranular storage of 5-HT, dopamine and NA is dependent on the maintenance of a pH-gradient across the granular membrane as well as on the granular membrane potential; (b) the ionophores cause a non-exocytotic release of granular amines, and (c) blood platelets are partial models for aminergic brain neurones as far as intragranular amine storage is concerned.

Animals↗
PubMed1989

Effects of capsaicin desensitization on the stimulatory effect of kinins, prostaglandins, biogenic amines and various drugs in guinea-pig isolated atria.

1. A simple desensitization protocol was set up using capsaicin and isolated, spontaneously beating atria of guinea-pigs to assess the possible participation of cardiac, capsaicin-sensitive, substance P (SP)- and calcitonin gene-related peptide (CGRP)-containing sensory nerve fibres, in the cardiac stimulatory effects of bradykinin (Bk), kallidin (Kd), 5-hydroxytryptamine (5-HT), histamine, prostaglandin E2 (PGE2), prostaglandin E1 (PGE1), prostaglandin F2 alpha, (PGF2 alpha), adrenaline (Ad), glucagon, nicotine and angiotensin II (AII). 2. The positive chronotropic and inotropic effects of Bk, Kd and 5-HT were markedly reduced in capsaicin-desensitized atria compared to control. The percentage inhibition of the chronotropic and inotropic responses to the three agonists seemed to be inversely related to the concentration of agonist used and to vary also with the type of cardiac effect produced by the drug (for Bk the percentage inhibition was: 36-81% (chronotropic effect) and 62-86% (inotropic effect); for Kd: 61-78% (chronotropic effect) and 53-77% (inotropic effect); for 5-HT: 25-66% (chronotropic effect) and 40-64% (inotropic effect]. 3. The positive chronotropic and inotropic effects of histamine, PGE1, PGE2, PGF2 alpha, glucagon and AII had similar amplitudes in capsaicin-desensitized and control atria. 4. The positive chronotropic and inotropic effects of Ad and nicotine were differentially affected by capsaicin desensitization. The inotropic effects of 7.5 x 10(-7) and 7.5 x 10(-6) M Ad were reduced by 41 and 27% respectively, in capsaicin-desensitized atria compared to control. The chronotropic effects of 1.54 x 10(-5) and 6.17 x 10(-5) M nicotine were inhibited by 57 and 26% respectively, by capsaicin desensitization. On the other hand, the chronotropic effect of Ad and the inotropic action of nicotine were of similar amplitude in capsaicin-desensitized and control atria. 5. These results were taken as an indication that a substantial part of the chronotropic and inotropic effects of Bk, Kd or 5-HT in guinea-pig atria, unlike those of histamine, PGE1, PGE2 PGF2 alpha, glucagon and AII, might be the result of stimulation of capsaicin-sensitive, SP- and CGRP- containing sensory nerve fibres. The slight, differential inhibition of the chronotropic and inotropic effects of Ad and nicotine by capsaicin desensitization suggests a minor contribution by cardiac, capsaicin-sensitive sensory nerve fibres to the effects of nicotine and Ad in guinea-pig atria.

Animals↗
PubMed1983

A study of urinary excretion of biogenic amine metabolites in epilepsy.

Urinary total catecholamines, their metabolites, and a metabolite of serotonin have been investigated in 20 patients with epilepsy, and in 10 controls. The levels of total catecholamines, vanillyl mandelic acid and 5-hydroxyindole acetic acid in epileptics were not significantly different from the controls. However, the mean 3-methoxy-4-hydroxyphenylglycol, excretion in cases of epilepsy was significantly increased as compared to the control group. It is concluded that a central catecholaminergic disturbance is involved in the pathogenesis of epilepsy.

Adolescent↗
PubMed1989

Biogenic amine metabolites in human CSF after hypoxia due to cardiac arrest.

The concentrations of 3-methoxy-4-hydroxyphenylglycol (MHPG), 5-hydroxyindole-3-acetic acid (5-HIAA) and homovanillic acid (HVA) were determined in CSF of patients with hypoxia due to circulatory arrest. Patients were divided into neurologically disabled and recovered according to the Glasgow Coma Scale. CSF was collected 4, 28, 76 and 172 h after commencement of resuscitation and once from control patients subjected to spinal anaesthesia. The initial concentrations of MHPG, 5-HIAA and HVA were significantly higher in a subgroup of neurologically disabled patients who died within 76 h. In recovered patients the concentration of MHPG declined with time to the value of the control group, whereas it increased in neurologically disabled patients. In the latter group the concentration of 5-HIAA also showed an increase with time, whereas in recovered patients it declined after an initial rise. It is concluded that high concentrations of MHPG, 5-HIAA and HVA in CSF may be prognostic for hypoxic brain injury after cardiac arrest.

Aged↗
PubMed1993

Biogenic amine metabolites in the CSF of patients with late onset and alcoholic ataxias.

The levels of monoamine metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxy-4-hydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA) were measured in lumbar cerebrospinal fluid (CSF) from 10 patients with late onset ataxia, 8 patients with alcoholic ataxia and 18 control patients. The levels did not differ significantly among the three groups of patients suggesting that the central neuronal systems utilizing dopamine, noradrenaline and 5-hydroxytryptamine do not have a significant pathophysiological role in these forms of ataxias. The measurement of CSF amine metabolites probably does not contribute to the differential diagnosis of ataxias.

Adult↗
PubMed1985

Effects of amiflamine and related compounds on the accumulation of biogenic monoamines in rat brain slices in vitro and ex vivo in relation to their behavioural effects.

The inhibition of the accumulation of serotonin, noradrenaline and dopamine in rat brain (occipital cortex and striatum) slices by amiflamine and its two major metabolites FLA 788(+) and FLA 668(+) was examined and compared with that of amine releasing compounds e.g. p-chloroamphetamine (PCA) and alpha-ethyltryptamine and uptake inhibitors, e.g. alaproclate, citalopram, desipramine, fluoxetine and norzimeldine. It was found that amiflamine and FLA 788(+) inhibited the accumulation of serotonin and noradrenaline but only slightly that of dopamine in vitro and ex vivo with a mechanism similar to that of PCA and alpha-ethyltryptamine, i.e. with higher potency in reserpinized rats than in normal animals suggesting amine releasing mechanisms. Similar to alpha-ethyltryptamine and PCA, amiflamine and FLA 788(+) caused behavioural changes (serotonin syndrome) which were particularly pronounced in reserpinized rats but also observed after a second administration of amiflamine in normal rats. Upon repeated administration of amiflamine the behavioural changes disappeared which indicates a functional down-regulation of the serotonin receptors responsible for this syndrome. FLA 668(+) inhibited the accumulation of noradrenaline in vitro and ex vivo but had less effect on the accumulation of dopamine and particularly that of serotonin. It is concluded that amiflamine and FLA 788(+) inhibit the accumulation of serotonin and noradrenaline by releasing mechanisms and that the released serotonin triggers the behavioural changes observed.

Animals↗
PubMed1984

Cation exchange--a common mechanism in the storage and release of biogenic amines stored in granules (vesicles)? III. A possible role of sodium ions in non-exocytotic fractional release of neurotransmitters.

The matrices of the amine storing granules in mast cells, chromaffin cells and noradrenergic nerves show properties reminiscent of cation exchanger materials. In vitro, the amines are released from their granule storage sites on exposure of the granules to cations, e.g. sodium ions. The proposal is made that also in vivo the release of transmitter amines is the result of cation exchange Amine+ in equilibrium Na+ ions and that the release of transmitter amines occurs as a nonexocytotic fractional release engaging multiple granules instead of exocytotic emptying of a few. Some physiological and pharmacological implications of a fractional transmitter release are discussed.

Adrenergic Fibers↗
PubMed1976

Alpha-methyl derivatives of biogenic amines as inhibitors of monoamin oxidase.

The values of Km app and Vmax for three natural substrates of monoamine oxidase have been determined at various stages in the isolation of the enzyme from rat liver tissue. The results are consistent with the presence in the enzyme preparation of at least two distinct molecular forms of the enzyme. Using the alpha-methyl derivatives of the natural substrates as inhibitors of the enzyme, the substrate dependence of Ki further substantiates this view. In addition, the kinetics of the inhibition suggest that the value of Km app may not for all substrates, necessarily be a measure of the affinity of the substrate for the enzyme.

Amphetamines↗