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

1. Dopamine amantadine and amphetamine have been applied directly by microiontophoresis to single neurones in the caudate nucleus and cerebral cortex of rats anaesthetized with urethane. 2. The predominant response to all three agents was a depression of neuronal firing rate. The responses to dopamine and amantadine could be antagonized by the dopamine receptor blocking agent, chlorpromazine. 3. Amantadine did not cause any potentiation of dopamine responses, suggesting that inhibition of amine uptake was not responsible for its effects. 4. The responses of pyramidal tract cells in the cerebral cortex to dopamine, amphetamine and amantadine were compared in control groups of rats and rats pretreated with reserpine (10 mg/kg i.p.) or alpha-methyl-p-tyrosine methyl ester (200 mg/kg i.p.). The reduction of cortical catecholamine concentrations was confirmed by a direct fluorimetric assay method. 5. Responses to dopamine were unaltered in the amine-depleted animals compared with controls. Responses to amantadine and amphetamine were reduced but not abolished. 6. It is concluded that amantadine acts partly by releasing catecholamines from neuronal stores. The residual responses to amantadine and amphetamine may be the result of a direct postsynaptic receptor stimulation.
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PMID:Responses of neurones in the cerebral cortex and caudate nucleus to amantadine, amphetamine and dopamine. 125 58

The acute administration of 4-chloroamphetamine caused a marked reduction in the concentration of serotonin and 5-hydroxyindoleacetic acid and a rise in dopamine in the rat brain. Following the injection of 3H-tyrosine and 3H-tryptophane into rats treated with 4-chloroamphetamine, there was a reduction in brain levels of 3H-dopamine and 3H-serotonin. Although the endogenous concentration of noradrenaline was not affected by 4-chloroamphetamine, there is evidence that its reuptake into neurones was reduced and its release increased by the drug. Following the administration of 4-chloroamphetamine for 10 days, the concentration of 5-hydroxyindoleacetic acid was reduced; no other changes in amine metabolism were apparent. From this investigation, and those of others, it appears that following acute administration, 4-chloroamphetamine has a neurochemical profile which has a similarity to that of many tricyclic antidepressants. However, there is a marked discrepancy between the acute and chronic effects of 4-CA on brain amine metabolism. Such findings are difficult to reconcile with the widely accepted theory that antidepressant drugs counteract the symptoms of depression by increasing the concentration of noradrenaline and/or serotonin at receptor sites within the brain.
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PMID:Acute and chronic effects of 4-chloroamphetamine on monoamine metabolism in the rat brain. 125 60

The present experiments were undertaken to determine, using Laser Doppler flowmetry, if elimination of efferent constrictor mechanisms would unmask cutaneous vasodilator responses following preganglionic sympathetic nerve stimulation in the forepaw of anesthetized cats. We also addressed the question of a potential causal relationship between neurally evoked vasodilator and sudomotor responses. Three separate anti-adrenergic regimens were utilized: (1) acute guanethidine administration (1-2 mg/kg); (2) chronic monoamine depletion with reserpine (5 mg/kg) and alpha-methyl-para-tyrosine (2 x 300 mg/kg); and (3) alpha-adrenoceptor blockade with prazosin (300 micrograms/kg) and yohimbine (0.5 mg/kg). Guanethidine treatment produced a significant depression of basal cutaneous blood flow whereas alpha-adrenoceptor blockade did not. In all three groups, stimulation of the preganglionic thoracic sympathetic nerve trunk produced intensity-dependent increases of digital skin blood flow along with near-maximal sympathetic-cholinergic sudomotor (electrodermal) responses recorded simultaneously from the same paw. Vasodilator responses were not altered by intravenous propranolol (1 mg/kg) or atropine (1 mg/kg); however, evoked sudomotor responses were totally blocked by atropine. Low doses (1.5 mg/kg i.v.) of hexamethonium selectively abolished the cutaneous vasodilator responses but not concomitantly evoked sudomotor responses. These results demonstrate, using direct measurements of blood flow, that cutaneous digital vasodilation can be measured in cats following removal of vasoconstrictor mechanisms either pre- or postjunctionally. Neither muscarinic nor beta-adrenoceptor mechanisms appear to be involved. These experiments also suggest that cutaneous vasodilation is not a consequence of concomitant sudomotor activation.
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PMID:Neurogenic cutaneous vasodilation in the cat forepaw. 135 May 98

Catecholaminergic pathways in the brain are activated during stress and are presumably involved in the control of physiological and behavioral changes triggered by stress. When repeatedly stressed, adaptive changes have been observed in catecholaminergic activity in the brain. In the present experiment, it was assessed whether or not chronic exposure to immobilization (IMO) altered the influence of catecholamines on behavior in the holeboard and forced swim test by administering alpha-methyl-p-tyrosine (an inhibitor of catecholamine synthesis). Adult Sprague-Dawley rats were used. Chronic stress amortiguated the inhibitory effect of acute IMO on some but not all behaviors in the two tests. Whereas previous chronic IMO exacerbated the effects of the drug on struggling and immobility in the forced swim test, no change in response to the drug as a consequence of chronic IMO was observed in the holeboard test. The present data suggest that chronic IMO-induced changes in the catecholaminergic control of some behaviors might be related to depression-like states in rats. The actual physiological meaning of these changes and the specific receptors involved remain to be elucidated.
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PMID:Inhibition of catecholamine synthesis depresses behavior of rats in the holeboard and forced swim tests: influence of previous chronic stress. 135 82

6R-L-erythro-5, 6, 7, 8-Tetrahydrobiopterin (6R-BH4) is known as a cofactor for the hydroxylases of phenylalanine, tyrosine and tryptophan and also as a cofactor for nitric oxide synthase. Recently, a novel function of 6R-BH4 has been found: that is, 6R-BH4 acts on specific membrane receptors to directly stimulate the release of monamine neurotransmitters such as dopamine and serotonin, independently of its cofactor activity. In addition, it indirectly stimulates the release of non-monoamine neurotransmitters such as acetylcholine and glutamate, through activation of monoaminergic systems. In this paper, we briefly review recent experimental data, which provide new insights into the role of 6R-BH4 as a regulator of neuronal function. We also discuss the possibility of treatment by 6R-BH4 of neuropsychiatric diseases such as Parkinson's disease, Alzheimer's disease, depression and infantile autism.
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PMID:[A novel function of tetrahydrobiopterin]. 136 Nov 76

The effects of dermorphin on EEG and autonomic variables are compared with the effects of 2 analogues and 2 homologues, all administered intracerebroventricularly in the rabbit. Dermorphin was the most effective in modifying all considered parameters: increase of cortically derived and calculated total power, bradycardia, respiratory depression and hypothermia. The dibenzylated heptapeptide was essentially inactive. The electrocortical pattern induced by the administration of L-dermorphin suggests a functional correlation between the amino acid D-ala 2 and the effects on EEG. Comparison between the effects produced by the N-terminal tetrapeptide and pentapeptide led us to hypothesize that amino acid Tyr 5 may be specifically involved in inducing the autonomic effects.
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PMID:Quantitative EEG and autonomic patterns of synthetic peptides related to dermorphin. 136 72

The study concerned 72 schizophrenic and 200 depressed patients hospitalised between 1983 and 1990. The erythrocyte membrane transports (EMT) of L-tyrosine and L-tryptophan (at 37 degrees, 0 degrees and 37-0 degrees) of schizophrenics without treatment nor depression were different compared to controls and depressed patients. The schizophrenics under neuroleptic treatment and/or depressed showed same means of EMT values as depressed patients. The slopes of the correlations between EMT of tyrosine or tryptophan at 37 degrees, 0 degrees and 37-0 degrees, as well as that between plasma levels of these amino acids, were parallel. However the slopes of the correlations between EMT of tyrosine and tryptophan were different according to the subgroups of patients: the perturbations of EMT were related to the clinical characteristics. In depressed patients and in schizophrenic patients under neuroleptic treatment and/or depressed, little changes in EMT of tyrosine were related to high changes of EMT of tryptophan.
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PMID:[Erythrocyte membrane transport of amino acid precursors of monoamines in schizophrenic patients. Comparison with depressive patients]. 136 21

In a previous paper evidence was presented to show that Helicobacter-induced chronic gastritis is the probable cause of most chronic hypochlorhydria. In this article evidence is presented for the clinical relevance of reduced stomach acid secretion. Reduced mineral absorption is fairly well documented and has sound theoretical support from basic chemistry. Impaired digestion of protein has been suggested by a few studies. Small intestinal bacterial overgrowth in hypochlorhydria probably leads to putrefactive breakdown of the metobolically useful products of protein digestion, thereby reducing their availability for certain essential pathways. The possible lowering of tryptophan, tyrosine, and phenylalanine in the blood may be a precipitating factor in depression in hypochlorhydric patients. In reduced or absent stomach acid secretion a constellation of gastrointestinal symptoms has been consistently observed and reported by clinicians in the past, and treatment of the hypochlorhydria with hydrochloric acid or its substitutes has often been observed to be effective in reducing these symptoms.
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PMID:The clinical importance of hypochlorhydria (a consequence of chronic Helicobacter infection): its possible etiological role in mineral and amino acid malabsorption, depression, and other syndromes. 149 27

The possible role of amino acid availability and a functional hypothalamic-pituitary-adrenal axis in the mood disturbances often reported in postpartum women and in users of the oral contraceptive was examined by measuring amino acids and doing a dexamethasone suppression test. Plasma cortisol, tryptophan, tyrosine, their competing amino acids in brain uptake (CAA), and the effect of 1mg dexamethasone were determined in 10 women taking oral contraceptives, 31 women 3 days postpartum, and 9 controls. The pill contained 30 mcg ethinyl estradiol and .075 mg gestodene (2 women), and 30 mg ethinyl estradiol and .15 mg desogestrel (8 women). The subject also took self-rating mood scales: Zung Depression, Zung Anxiety, Beck Depression and State Anxiety Inventory. Cortisol was significantly higher in postpartum women and pill users than in normal controls. Tryptophan, valine, isoleucine and leucine were lower in postpartum women. Tyrosine and tyrosine CAA were lower in postpartum women and pill users. 80% of the postpartum group had negative dexamethasone suppression tests, i.e., cortisol 5 mcg/dl 24 hours after 1 mg dexamethasone. After dexamethasone valine was significantly higher and tryptophan/CAA and tyrosine/CAA ratios were lower, as a result of slightly lower tryptophan and tyrosine and slightly higher CAAs. Furthermore, effects on the amino acid ratios were only evident in women exhibiting dexamethasone suppression. There was a significant negative correlation between depression and anxiety scores and the tryptophan/CAA ratio. The results indicated first that the dexamethasone suppression test is an invalid marker for major depression, and also that availability of the amino acid precursors of brain neurotransmitters may affect mood in the puerperium.
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PMID:Disturbances in dexamethasone suppression test and lower availability of L-tryptophan and tyrosine in early puerperium and in women under contraceptive therapy. 156 Apr 30

The effects on C fiber evoked activity in lumbar dorsal horn convergent neurones of i.v. morphine alone, of Tyr-D-Thr-Gly-Phe-Leu-Thr (DTLET) alone or of either of these drugs in association with 5-deoxyadenosylcobalamine (dibencozide) were investigated in anesthetized rats. Both morphine and DTLET depressed the neuronal responses in a dose-related fashion, with the former requiring lower doses. Although dibencozide alone was devoid of any effect, it significantly enhanced the depressive effects of all doses of morphine tested and of the lower two doses of DTLET. It is concluded that dibencozide enhances the spinal depression of nociceptive information elicited by mu and delta opioid agonists. This drug could provide a useful tool for the study of interactions between opioids and opioids receptors. It is also suggested that dibencozide could be useful in clinical practice for reducing the dosage of opioids.
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PMID:Depressive effects of mu and delta opioid receptor agonists on activities of dorsal horn neurones are enhanced by dibencozide. 164 26


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