Hypothesis of a deficiency of central noradrenergic input in DST nonsuppressor depressed patients. A clinical study with determination of DST and plasma DOPEG: negative results.
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Brain↗
Biomedical subjects
T Dennis
Publications and source records attributed to T Dennis.
Increase in dopamine and DOPAC levels in noradrenergic terminals after electrical stimulation of the ascending noradrenergic pathways.
The effect of electrical stimulation of the ascending noradrenergic neurons on the formation of dopamine and its major deaminated metabolite dihydroxyphenylacetic acid (DOPAC) in the hippocampal formation, a predominantly noradrenaline-rich brain area, has been investigated in the rat. Electrical stimulation of the locus coeruleus or ascending noradrenergic pathways caused a pronounced increase in hippocampal dopamine and DOPAC levels which paralleled the increase in free and conjugated dihydroxyphenylethyleneglycol levels. The elevation of hippocampal DOPAC was no longer seen after chemical lesion of the noradrenergic pathways. It is suggested that the enhanced formation of dopamine and DOPAC in hopocampal noradrenergic terminals under conditions of increased noradrenergic impulse flow may be connected to an inefficient beta-hydroxylation of dopamine to noradrenaline with a subsequent oxidative deamination of dopamine into its degradation products.
3,4-Dihydroxyphenylacetic Acid↗
[Study of noradrenaline metabolism in depressed patients by the determination of plasma dihydroxyphenylethylene glycol].
The plasmatic levels of free, sulfoconjugated and total dihydroxyphenylethyleneglycol (DOPEG), the main deaminated metabolite of noradrenaline, have been measured in thirty DSM3 major depressive inpatients and in thirty healthy controls matched for sex and age. DOPEG levels have been measured by a radioenzymatic assay. Almost fifty per cent of depressed inpatients were D.S.T. non suppressors, thirteen patients were unipolar and thirteen bipolar. Plasmatic DOPEG levels were significantly lower in depressed patients as compared to healthy controls despite a wide interindividual range of DOPEG values. However, the ratio of free over conjugated DOPEG was not statistically different in the two groups. DOPEG levels were slightly higher in the female population of healthy volunteers but not in the depressed patients. In the healthy volunteers, but not in depressed patients, there was a trend for free DOPEG to increase and for conjugated DOPEG to decrease with age. There was no statistical correlation between the DOPEG levels and Hamilton Depression Scores. Also plasmatic DOPEG values were not different in uni or bipolar patients and in DST suppressor or DST non suppressor inpatients. The significance of the decrease of plasmatic DOPEG levels in depressed patients is discussed: this diminution may reflect a deficiency in noradrenaline metabolism in CNS or else may be attributed to other factors e.g. alteration in circadian rhythms, differences in motor activity, in level of anxiety, in sleep and feeding behaviors; cotreatment with benzodiazepine and opiate compounds; monoamine oxidase activity.
Adult↗
A radioenzymatic technique for the measurement of free and conjugated 3,4-dihydroxyphenylethylene-glycol in brain tissue and biological fluids.
A simple, sensitive and specific radioenzymatic assay for the measurement of 3,4-dihydroxyphenylethyleneglycol (DOPEG) was developed. The assay is based on the conversion of the compound to its O-methylated derivative in the presence of catechol-O-methyltransferase and [3H]S-adenosyl-methionine. The tritiated 3-methoxy-4-hydroxyphenylethyleneglycol formed is selectively extracted in organic solvents and isolated by thin layer chromatography. After oxidation to vanillin the O-methylated compound is extracted and measured by liquid scintillation spectrophotometry. This assay has been applied to the measurement of free and conjugated DOPEG in a variety of biological tissues and fluids. Both free and conjugated DOPEG were readily detected in discrete rat brain areas. Substantial amounts of free and conjugated DOPEG were also measured in ventricular perfusates from freely moving rats. Finally, the presence of DOPEG was also demonstrated in human cerebrospinal fluid, plasma and urine. Only the free form of DOPEG was found in cerebrospinal fluid, whereas both unconjugated and conjugated forms were present in plasma and urine.
Animals↗
Nursing care study. Embryonic sarcoma: a brave child loses her fight.
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Child↗
Effects of clonidine, prazosin and phentolamine on heart rate and coronary sinus catecholamine concentration during cardioaccelerator nerve stimulation in spinal dogs.
1 In spinal dogs, continuous electrical stimulation of the cardioaccelerator nerve produced a transient rise in aortic blood pressure and a sustained increase in both heart rate and coronary sinus blood flow. The latter effects were accompanied by a significant elevation in the coronary sinus plasma noradrenaline concentration without significant changes in the levels of dopamine and adrenaline. The concentrations of the three catecholamines in thoracic aorta plasma were not significantly changed by cardioaccelerator nerve stimulation.2 Clonidine (20 mug/kg, i.v.), given during cardioaccelerator nerve stimulation, increased both mean aortic blood pressure and coronary sinus blood flow and decreased heart rate and coronary sinus venous plasma noradrenaline overflow.3 Phentolamine (0.3 mg/kg, i.v.) completely antagonized these effects of clonidine. Prazosin (0.3 mg/kg, i.v.) inhibited by only 43 and 38% the respective reductions in heart rate and noradrenaline overflow elicited by clonidine.4 On termination of cardioaccelerator stimulation (about 10 min after either prazosin or phentolamine), heart rate and coronary sinus noradrenaline overflow returned to control prestimulation levels.5 Phentolamine or prazosin, administered alone during stimulation of the cardioaccelerator nerve, increased heart rate and noradrenaline overflow into the coronary sinus plasma. However, intravenous phentolamine and prazosin, in contrast to desipramine (0.3 mg/kg, i.v.) or tyramine (1.0 mg, i.a.), failed to change the tachycardia resulting from the local administration of noradrenaline into the sinus node artery (i.a.).6 These results show that in spinal dogs the clonidine-induced reduction in heart rate (elevated by electrical stimulation of the cardioaccelerator nerve) is accompanied by a fall in the quantity of noradrenaline overflowing into the coronary sinus plasma. The latter effect is presumably the result of an action of clonidine on cardiac presynaptic alpha-adrenoceptors, the activation of which is followed by a reduction in the release of noradrenaline per nerve impulse. Phentolamine and prazosin are both antagonists of cardiac presynaptic alpha-adrenoceptors in spinal dogs, as suggested by their action against clonidine and by their positive chronotropic effect when administered during stimulation of the cardioaccelerator nerve.
Animals↗