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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of neurones in the substantial nigra and ventral tegmentum was recorded extracellularly in vitro. Dopamine produced depression of spontaneous firing in a dose-dependent manner. Antagonism of these neuronal responses to dopamine by metoclopramide, SCH 23390 and clozapine was examined. Metoclopramide antagonised the responses to dopamine in the manner expected; SCH 23390 had little effect on the response to dopamine as would be predicted for a selective dopamine "D1" antagonist. Clozapine did not produce the expected antagonism of the response to dopamine. The results at the single neurone level are compared with behavioural and biochemical data.
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PMID:Sensitivity of neuronal dopamine response in the substantia nigra and ventral tegmentum to clozapine, metoclopramide and SCH 23390. 329 79

Different neurotransmitters (Dopamine, serotonin, GABA...) and hormones (TRH, oestrogenes...) are involved in the central regulation of prolactin synthesis and release. Under physiological conditions, prolactin levels are related to correlate with age, sex, sexual maturational changes (puberty, menopause...), menstrual cycling... In this review of literature there exists a great amount of data concerned with changes in prolactin in affective disorders illustrating the validity of the biochemical and neuroendocrinological approach specially in depression. Different research paradigms are presently reviewed: measurement of plasma levels of prolactin under basal conditions, in a circadian pattern or after pharmacological challenge with TRH and/or morphine (stimulation), L-dopa and/or dexamethasone (inhibition) and its response to antidepressant drugs. The authors emphasize the contradictory results reported in the literature and suggest the need for extreme caution before considering the validity of prolactin as a biochemical test in depression.
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PMID:[Prolactin, depression and antidepressive agents. Review of the literature]. 329 33

Synaptic transmission between mechanosensory and motor neurons of the gill withdrawal reflex in Aplysia can undergo both short-term and long-term modulation. One form of short-term synaptic depression lasting minutes can be evoked by the peptide Phe-Met-Arg-Phe-amide (FMRFamide), and is mediated by the lipoxygenase pathway of arachidonic acid. We report here using cell culture, that the same monosynaptic sensory-to-motor component of the gill withdrawal reflex can also undergo long-term synaptic depression lasting 24 h after five applications of FMRFamide over a 2-h period. The long-term depression evoked by FMRFamide is transmitter-specific. Dopamine or low-frequency stimulation of sensory neurons, which also produce short-lasting synaptic depression in vivo, failed to evoke a long-term change. As is the case for long-term presynaptic facilitation of this connection with serotonin, the long-term depression, but not the short-term, can be blocked when applications of FMRFamide are given in the presence of anisomycin, a reversible inhibitor of protein synthesis. Thus, heterosynaptic depression parallels heterosynaptic facilitation in having a long-term as well as a short-term form, and in both cases the long-term modulation requires the synthesis of gene products not essential for the short-term changes.
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PMID:Long-term heterosynaptic inhibition in Aplysia. 336 86

To investigate the effect of intravenous dopamine on the chemical regulation of ventilation, we studied the ventilatory responses to hypercapnic hypoxia during dopamine infusion. Intravenous dopamine (3 micrograms X kg-1 X min-1) was administered to six healthy human subjects. Two hypoxic challenges (PETO2 = 52.5 +/- 2.5 mm Hg, SaO2 = 88.8 +/- 2.2%; mean +/- SD) were administered at three CO2 levels (PETCO2 = 40.8 +/- 0.5, 45.6 +/- 0.2, 49.8 +/- 0.3 mm Hg) to each subject. The ventilatory responses were quantified by calculation of slopes and intercepts of the relationship between minute exhaled ventilation (VE) and arterial hemoglobin saturation (SaO2), and by the relationship between this slope (delta VE/delta SaO2) and carbon dioxide tension. Dopamine caused a 77% reduction in delta VE/delta SaO2 (hypoxic sensitivity) during eucapnia, a 39.5% reduction in hypoxic sensitivity at PETCO2 = 46 mm Hg, and 38% reduction at PETCO2 = 50 mm Hg (P less than 0.05). Dopamine also reduced normoxic ventilation at all carbon dioxide levels. There was a greater depression in VE during hypercapnia (25.7% reduction) than during eucapnia (12% reduction). This indicates that dopamine depresses the normoxic ventilatory response to carbon dioxide. Intravenous dopamine reduces the ventilatory response to both hypoxia and hypercapnia but preserves the augmentation of hypoxic ventilatory drive by hypercapnia.
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PMID:Effect of dopamine on hypoxic-hypercapnic interaction in humans. 360 70

The acetylcholine turnover rate and the enzymatic activity of choline acetyltransferase were determined in the nucleus accumbens and striatum. Whereas both apomorphine and a serotonin agonist MK 212 led to a decrease in acetylcholine turnover rate, haloperidol showed the opposite effect in the nucleus accumbens and striatum, respectively. Dopamine and serotonin agonists induced a depression of the enzymatic activity but this effect was less pronounced than the effect on acetylcholine turnover rate. It is concluded that in the nucleus accumbens and striatum the cholinergic interneurons appear to be modulated by dopaminergic and serotonergic systems in an inhibitory manner.
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PMID:Modulation by dopaminergic and serotonergic systems of cholinergic interneurons in nucleus accumbens and striatum. 383 17

Dopamine and apomorphine were injected directly into limbic, extrapyramidal and cortical areas of mouse brain to determine relative sensitivities to the inhibitory effects of these agents on mouse spontaneous climbing behaviour. Injections of 0.06-2 micrograms apomorphine or dopamine into the nucleus accumbens, central area of the amygdala, septum or ventral tegmental nucleus caused dose-dependent motor inhibition with maximal reductions in the order of 60-70% of control value. In the extrapyramidal nuclei, caudate-putamen and globus pallidus, apomorphine and dopamine were required at 0.5-2.5 micrograms to produce inhibition, but the degree of inhibition never achieved 50% of control. Apomorphine and dopamine (0.001-10 micrograms) failed to cause any inhibition of mouse spontaneous climbing behaviour when injected into the anteromedial, supragenual or suprarhinal cortex. The higher doses of dopamine or apomorphine could effect stimulation of climbing behaviour from the limbic, extrapyramidal and cortical areas. Bilateral injections of haloperidol or (-)sulpiride (0.001-1 microgram) into the selected limbic and extrapyramidal areas caused dose-related depression of mouse spontaneous climbing, the limbic areas, particularly the nucleus accumbens, being the most sensitive. Doses of these neuroleptics selected as having minimal effect in their own right were shown to antagonise the marked motor inhibition effected by dopamine and apomorphine from the limbic areas, and the modest inhibition effected from the extrapyramidal areas. In contrast, intracerebral pretreatments with prazosin or yohimbine failed to antagonise the motor inhibitory effects of dopamine or apomorphine from any brain area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dopamine agonist action in mesolimbic, cortical and extrapyramidal areas to modify spontaneous climbing behaviour of the mouse. 392 17

Amineptine is a new tricyclic compound with a grafted long aliphatic chain active on Dopamine synaptic release and as such more desinhibitor, safer and short acting. The study was coordinated by a national and 13 local counsellors. It was an open study. Inclusions criteria and results are examined, making obvious that patients responded well according to the Hamilton rating scale for depression (17 item version--16.4 points dropped at day 7th in 43%) and that it is an efficaceous antidepressant.
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PMID:[Value of amineptin in the treatment of different depressive states. Apropos of 112 cases treated as part of a national multi-centric study]. 408 4

In nine patients in anaerobic septic shock, five of them with hepatic injury compatible with sepsis liver failure, hematic chloramphenicol concentration was determined at 5 minutes, 1, 2, 3 and 6 hours after intravenous administration of the first of three daily dose (50 mg/k/day); in the hepatic failure group the procedure was repeated with the next dose, previous attempt of haemodynamic compensation with two hours dopamine (3-10 mcg/k/min.) infusion. Starting from experimental data computation adjustment of time-concentration curve and lineal regression with a p = 0.0001 adjustment was done, determining half live (HL), distribution volume (DV), constant of elimination (K) and clearance (CL). In septic shock without hepatic injury patient group, there was noticed a uniform behavior in time-concentration graphic, withdrawn from chloramphenicol bone-marrow depression levels and pharmacokinetics parameters quite near the normal ones, with a reasonable extension of (DV). When attempting hepatic injury patient group, though an individual variability, drug concentration reach bone marrow depression levels and there was a significant lowering of Cl (p = 0.001) and a reasonable one of DV. Dopamine haemodynamic compensation attempt results in an increase of chloramphenicol hematic concentration in the sepsis liver group and the pharmacokinetics levels bear new deterioration. Practical meaning of the methodology used in drug handling in severe hepatic failure is stressed, to allow mathematic valuation of different pathogenic compounds. Though each patient should be individually evaluated, in septic shock without liver injury chloramphenicol dosification should not been any changes but in presence of sepsis liver doses should be diminished to half and administration interval extended to 11.5 hours.
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PMID:[Drug metabolism in the septic liver: conclusions about the pharmacokinetics of chloramphenicol]. 409 Sep 20

1. Dopamine applied iontophoretically to neurones of the caudate nucleus of cats caused excitation of some (9% of those encountered) and depression of others (60%). Some cells have been found affected both by dopamine and by acetylcholine.2. The effects of dopamine could be prevented by the previous iontophoretic administration of phenoxybenzamine, but not by dichloroisopropylnoradrenaline.3. Responses evoked in caudate neurones by electrical stimulation of substantia nigra were depressed by dopamine. No evidence for enhancement of the effects of nigral stimulation through the application of dopamine were detected.4. Stimulation of nucleus centromedianus thalami depressed firing of caudate neurones.5. The hypothesis that dopamine may act as an inhibitory synaptic transmitter within the caudate is put forward.
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PMID:The action of dopamine on neurones of the caudate nucleus. 438 18

25% of patients with Parkinson's disease demonstrate the first symptoms with 70 years. The deficiency of Tyrosinhydroxylase is the trigger of the decreased level of Dopamin in the basal ganglia. The implications are the typical symptoms (tremor, rigor and akinesia) and the psychopathological decompensations as depression, delirs and bradyphrenie.
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PMID:[Senile Parkinsonism: its motor and psychological defects]. 612 32


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