Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood platelet serotonin levels were measured in unmedicated 12 manic and 74 depressive patients with 118 normal control subjects employed. Blood platelets were separated by multiple contrifugation in the medium of Na2-EDTA solution, and the loss of serotonin during collecting procedures was about 11%. The mean value of blood platelet serotonin levels in depressed patients was 594+/-288ng/mg platelet protein (+/- S.D.), which was significantly lower than that for normal controls, 780 +/- 253ng/mg protein (p less than 0.001). Age does not account for the reduction of serotonin levels both in depressed and in normal population. Unipolar and involutional depressed patients exhibited to have the most pronounced reduced levels of serotonin of various subtypes of depression, while bipolar depressed patients, neurotic and chronic characterological depressed patients as well as patients with first-episode depression had the values which were comparable with those in normal controls. Manic patients did not show enhancement but did reduction of serotonin levels, the mean being 580+/-152ng/mg protein, which made a contrast with their clinical manifestations of exhilaration and hyperactivity. Changes in blood platelet serotonin levels were determined before, during and after administration of L-5-HTP with a maintenance dose of 300mg daily in nine depressed patients. Serotonin levels in all subjects were lifted to normal levels during the L-5-HTP treatment, while clinical symptoms were not improved with the treatment. Reduction of blood platelet serotonin levels in depressed patients may be due to their psychobiological distinction, which involves abnormal biogenic amine metabolism in the brain.
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PMID:Reduction of blood platelet serotonin levels in manic and depressed patients. 108 14

A series of studies of monoamines and their metabolism in a variety of human tissues indicate that there are aging effects that may alter neurotransmitter substances. Monoamine oxidase (MAO) activity has a significant positive correlation with age in plasma and blood platelets of normal subjects and patients suffering from depressive disorders. Monoamine oxidase and age correlate positively in hindbrain and in eight separate ares of human brains from patients who died from a variety of causes. Hindbrain norepinephrine concentration progressively decreases with advancing age (r equals -0.44, P less than 0.01) while no changes were noted for serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA). Hindbrain norepinephrine concentration has a significant negative correlation with MAO (r equals -0.41, P less than 0.025) and hindbrain 5-HIAA has a significant positive correlation with MAO (r equals +0.66, P equals less than 0.05). These studies suggest that aging processes may significantly affect monoamine mechanisms and be a predisposing factor to the development of clinical diseases in man such as depression, parkinsonism and other disorders of central nervous system homeostasis.
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PMID:Changes in monoamine oxidase and monoamines with human development and aging. 108 42

The effect of progesterone upon stress altered serotonin (5-HT) metabolism in various regions of the rat brain was investigated with regard to a possible connection with premenstrual and post-partum depression. When electric footshock was administered to ovariectomized rats pretreated with progesterone or its vehicle, there were generally higher 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) concentrations after progesterone. 5-HT levels were significantly higher in thalamus, hippocampus, raphe, and frontal cortex, 5-HIAA rose significantly in hippocampus, raphe, and frontal cortex. Whereas after electric footshock alone the septum showed highest increases of 5-HT and 5-HIAA and hippocampus ranged last, after pretreatment with progesterone increases of 5-HT and 5-HIAA were least pronounced in septum but rather high in hippocampus. Electric footshock administered to ovariectomized rats also resulted in an increase of plasma progesterone concentration.
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PMID:Influence of stress on regional brain serotonin metabolism after progesterone treatment and upon plasma progesterone in the rat. 112 Sep 48

Successive daily injections of LSD-25 and UML (1-methyl-d-lysergic acid butanolamide) caused progressive depression of brain 5-HT levels in the rat. On the fourth day, the decrease was significant with respect to the highly significant fall observed after a single administration, whereas it had been shown earlier that conditioned behaviour is no longer affected by LSD-25 after 3 days and that simultaneous administration of a single dose of LSD-25 and UML is equally ineffective in this respect. Its depression of 5-HT levels, however, has now been shown to be equal to that of LSD-25 alone at doses that influence conditioned behaviour. The findings indicate that changes in such behaviour are not dependent on brain 5-HT levels and that no link exists between such levels and the psychotomimetic effect of LSD-25 in man.
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PMID:The relation between cerebral serotonin levels and conditioned behaviour in the rat following the administration of LSD-25 and UML. 115 13

The effect of various doses of serotonin (5-HT) on the basal or insulin-stimulated gastric secretion was studied, for 4 hr after the injection, in unanesthetized rats with chronic gastric fistulas. The blood glucose and serum Na, K and Ca ions concentrations were also determined. Insulin produced hypoglycemia and hypokalemia, most pronounced in the first hr, and increased HCl and pepsin output, with a maximum at 2 hr after the injection. 5-HT significantly inhibited both basal and insulin-stimulated gastric secretion. The amine produced transient hyperglycemia, which was less pronounced in rats simultaneously receiving insulin. The inhibition of insulin-stimulated gastric secretion by 5-HT lasted for a longer period than the prevention of the biochemical changes brought about by insulin. The prevention by 5-HT of insulin hypoglycemia and hypokalemia may be of significant importance in the mechanism of the depression of insulin-stimulated gastric secretion.
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PMID:The influence of serotonin on insulin-stimulated gastric secretion, blood glucose and serum electrolyte levels in the unanesthetized rat. 116 2

A sensitive and specific procedure for measuring monoamine oxidase (MAO) activity in human platelets is described. Serotonin is used as substrate and formed 5-hydroxyindoleacetic acid (5-HIAA) is separated by a double microcolumn technique on Sephadex G-10 and Amberlite CG-50 and measured fluorimetrically. MAO activities were 5.11 +/- 1.32 (mean +/- S.D.) nmol/mg protein/hour in male and 7.85 +/- 1.58 in female healthy adults (p less than 0.001). MAO activity measured in 32 depressed patients was in a range of 3.20-10.62 nmol/mg protein/hour, the value not differing from that in the normal subjects. No significant difference was established between three subtypes of depression, in bipolar, unipolar and involutional patients, while significantly higher values were evident in female than in male patients (p less than 0.001).
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PMID:A sensitive non-isotopic assay for monoamine oxidase activity in human blood platelets. 116 8

By means of single unit recording techniques it was found that a small systemically administered (intravenous) dose of the alpha-adrenergic agonist clonidine inhibited the spontaneous firing of brain norepinephrine (NE)-containing neurons in the locus coeruleus. In addition, the NE neurons were consistently inhibited by the direct (microiontophoretic) application of minute amounts of NE or clonidine. Intravenous clonidine also inhibited the firing of the great majority of (5-HT) neurons in the midbrain dorsal raphe nucleus. However, this action does not appearto be a direct one since clonidine (and NE) had relatively weak or variable effects when applied microiontophoretically to raphe neurons. The clonidine-induced depression of raphe firing may be secondary to an impairment in adrenergic transmission since (1) the depression could be reversed by the NE-releasing agents D- and L-amphetamine, (2) high doses of clonidine itself (which have been reported to have postsynaptic alpha-agonistic activity) reversed the depression produced by a low dose of clonidine and (3) prior destruction of NE neurons by 6-hydroxydopamine (7-12 days) rendered raphe neurons insensitive to the depressant effect of i.v. clonidine. Dopaminergic (substantia nigra, zona compacta) neurons did not respond to either low or high doses of clonidine. These results are consistent with previous data showing that clonidine decreases NE and 5-HT but not dopamine turnover. We conclude that systemically administered clonidine inhibits the firing of brain NE neurons by acting directly upon adrenergic receptors located on or near the soma of these neurons but that the concomitant inhibition of 5-HT neurons is an indirect effect (possibly secondary to an impairment in noracrenergic transmission).
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PMID:Inhibition of both noradrenergic and serotonergic neurons in brain by the alpha-adrenergic agonist clonidine. 117 54

Biochemical human post-mortem studies on depressed patients indicate an unspecific deficiency of neurotransmitters in several brain areas. The loss of drive of these patients could be correlated with a decrease of striatal dopamine concentration. Noradrenaline was significantly diminished in red nucleus, a fact which points to the characteristic posture of depressed patients. Serotonin was diminished in all brain areas. During remission all values trended to be normal. There also exists a circadian disrhythm in depressed patients resulting in lowered VMA- and HVA-levels in urines during the morning and a remission to normal values in the evening. This agrees with the findings of lowered blood tyrosine levels in the morning. The ratio of blood tyrosine and tryptophan is disturbed during depression and recovers during remission. Central and peripheral biochemical mechanisms seems to be involved in depression syndrom.
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PMID:Biochemical post-mortem findings in depressed patients. 118 63

The functions of the central monoamines Norepinephrine (NE) and Serotonin (5HT) can be clarified by the study of behaviors of rats administered selective monoamine toxins. In his home environment the low NE rat has drive deficits and is lethargic, tending to remain in his burrow, but in novel environments this animal acts less frightened than Controls. The low 5HT rat is conversely active and exploratory in familiar environments but frightened in novel environments. These two animals model aspects of depression and anxiety, respectively. 5HT can be thought of as placing the brain into a state of consciousness appropriate for an animal in his nest (i.e., 5HT neurons act as relaxers), and as involved in a type of positive affect related to security, whereas NE neurons are dominant when an animal is vigilant, foraging out in the environment and are involved in a type of positive affect related to goal-directed approach arousal. Monoamine toxins may be produced when the behaviors elicited by these central neuronal systems are negatively reinforced (extinguished).
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PMID:Behavior and the balance between norepinephrine and serotonin. 123 10

We have examined the effects of two monoamine oxidase (MAO) inhibitors with different mechanisms of action--phenelzine and brofaromine--on peripheral serotonergic (5-hydroxytryptamine [5-HT]) measures, sensitive to the inhibition of MAO-A (intra- and extracellular 5-HT and related metabolites in blood). Both drugs increased the concentration of 5-HT in platelet-free plasma (254%, p less than 0.001) in patients with depressive illness (DSM-III-R) after 6 weeks of daily treatment. Platelet 5-HT was also increased significantly in both drug treatment groups but more marked in the patient group treated with phenelzine. The acid/amine ratio at 6 weeks was 30% of pretreatment values (p less than 0.000) and individual variability correlated significantly with the Hamilton Rating Scale for Depression. Plasma 5-HT increased more markedly in responders than in nonresponders and a significant inverse relationship surfaced between plasma 5-HT and the Hamilton Rating Scale for Depression. The results support other reports of comparable antidepressant efficacy for brofaromine and phenelzine, both inhibitors of MAO-A in humans. The consistent relationship we found between the biochemical and clinical changes again suggests and supports a key role of 5-HT in the antidepressant effect of these MAO inhibitors.
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PMID:Monoamine oxidase inhibitors phenelzine and brofaromine increase plasma serotonin and decrease 5-hydroxyindoleacetic acid in patients with major depression: relationship to clinical improvement. 128 22


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