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

In an experimental study we tried to find out whether halothane, in addition to its effects on vegetative efferents, has also an influence on catecholamine metabolism of the corresponding brain sections. We studied the effects of halothane in the brain stem of rats on dopamine and norepinephrine contents and on the transformation of L-dopa into dopamine and L-norepinephrine. Anaesthesia with 2 vol% halothane reduced dopamine content by 41.4%, norepinephrine content by 17.8%. These findings could be observed even 3 h after narcosis. Electrophysiological studies show that the central nervous sympathetic activity at rest and after central excitation is clearly reduced during anaesthesia with 2 vol% halothane; 70 min after narcosis it returned to normal. Administration of L-dopa led to an increase of dopamine by 43.5% within 45 min. This transformation of L-dopa into dopamine is not affected by concurrent halothane anaesthesia. There is no increase in norepinephrine after administration of L-dopa. Thus, the effect of halothane on catecholamine metabolism in the brain stem affects the precursors of L-dopa. Halothane is said to inhibit transport of the L-dopa precursor L-tyrosine from plasma to brain tissue. Along with such an inhibition goes the depression of the sympathetic activity. In this respect and obviously on the basis of its position within the catecholamine metabolism, dopamine is more important than norepinephrine.
 ...
PMID:[Effect of halothane on catecholamine metabolism in the brain stem of rats]. 98 21

Keeping in mind the vasodilator action of prostaglandins, the control that they exercise over the vascular supply of kidneys and the sympathetic activity, research was conducted in order to establish the effect of arachidonic acid, the precursor of PGE2, on experimental hypertension in the rat. The experimental hypertension was induced by unilateral nephrectomy, followed by the administration of DOCA and the elevated sodium diet. The treatment was short in one group, long in the other, and both groups were compared to a control hypertensive group which received no treatment at all. Arachidonic acid worsened the experimental hypertension by 37% in the long treatment, and by 25% in the short treatment. The administration of lysine-acetylsalicylate diminished this hypertension. A non-saturated acid, oleic acid, which is not involved in prostaglandin synthesis, has no action. The authors would like to emphasize that in one of the previous experiments, L-tyrosine, the precursor of catecholamines, diminished the experimental hypertension in the rat, and also that L-DOPA and IMAO (MAOI) have comparable effects. It seems, therefore, that the depression of the central catecholaminergic activity, which is supposed to be the action of arachidonic acid via an increase in the PGE2 synthesis, appears to increase hypertension. It is noteworthy that the medial forebrain bundle (MFB) is catecholaminergic and that the periventricular system (PVS) is cholinergic. Thus hypertension may represent the peripheral vascular response to anguish which results from the activation of PVS and from the depression of MFB.
 ...
PMID:The action of arachidonic acid on experimental hypertension in the rat. 112 60

We have reported earlier that administration of 3-nitro-L-tyrosine (MNT), 8 mM in drinking water, to rats receiving a low iodine diet (LID) results in greater TSH secretion, larger goiters, and more rapid uptake and release of radioiodine than LID alone, and ultimately may produce hypothyroidism. These findings have been confirmed, and hypothyroidism documented by demonstrating depressed levels of hepatic mitochondrial alpha-glycerophosphate dehydrogenase. Also, prolonged treatment with MNT + LID produced a depression in labeled iodothyronine (ITh) synthesis, as judged by chromatographic analysis of thyroid digests from rats killed 4 or 24 hours after ip injection of radioiodine, or two weeks after adding radioiodine to drinking fluid. Low thyroidal ITh levels were accompanied by low levels of ITh in serum, despite the presence of various other labeled organic iodine compounds. Cessation of MNT treatment, or ip injection of small amounts (0.5-1.0 mug) of Na 127I together with radioiodine 4 h before sacrifice reversed the defect, and large amounts of ITh were found in both thyroid and serum. Labeled thyroprotein from MNT-treated rats showed increased susceptibility to disaggregation during freezing at pH 8.5; this abnormality was also reversed by stable iodine treatment. In glands labeled with radioiodine 24 h before sacrifice, stable iodine injection 20 h later was followed by increased thyroidal ITh. It is concluded that profound iodine deficiency, induced by MNT + LID, can lead to diminished ITh synthesis, or a "coupling defect". The results provide an explanation for the finding of low thyroidal ITh in patients with hereditary deficiency of tyrosine dehalogenase. The findings confirm an important role for iodine supply in ITh synthesis and thyroglobulin stability, and suggest that rats treated with MNT + LID provide a model for study of the effects of extreme iodine deficiency.
 ...
PMID:Induction of a coupling defect in rats during inhibition of tyrosine dehalogenase. 124 38

Recent experimental data are summarized about changes in the functioning of calcium ion channels in clonal cellular lines (pheochromocytoma PC12) and hippocampal neurons of newborn rats on the background of altered intracellular level of aromatic amino acid L-tyrosine or its precursors L-phenylalanine. Elevation of the level of L-phenylalanine persistently down-regulated the high-threshold voltage-operated calcium channels in both types of cells without affecting the low-threshold ones in hippocampal neurons. This depression could be to some extent reversed by elevation of the level of L-tyrosine. Thus both amino acids seem to exert a long-lasting antagonistic modulatory effect on the corresponding channels, mediated probably through changes in tyrosylation of some cytoskeletal proteins. The participation of these molecular mechanisms in brain dysfunction during congenital disease phenylketonuria is suggested.
 ...
PMID:[Possible molecular mechanisms of brain dysfunction in phenylketonuria]. 130

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.
 ...
PMID:[Erythrocyte membrane transport of amino acid precursors of monoamines in schizophrenic patients. Comparison with depressive patients]. 136 21

In the treatment of depression, when antidepressant drug choice is made according to alterations of erythrocyte membrane transport of L-tyrosine and L-tryptophan in the individual patient, the clinical results are superior to those obtained when drugs are prescribed according to the physician's judgment. This is demonstrated by comparing three experimental groups: I, 100 patients treated in relation to their L-tyrosine and L-tryptophan transport; II, 30 patients treated according to the clinician's experience; III, 38 subjects treated against the L-tyrosine and L-tryptophan transport indications. In these groups, the frequency of patients improved by more than 70% is 77%, 47%, and 16%, respectively.
 ...
PMID:L-tyrosine and L-tryptophan membrane transport in erythrocytes and antidepressant drug choice. 215 54

The two most widely held biochemical models of depression--the catecholamine (CA) and indoleamine (IA) hypotheses--explain depression as a result of deficient transmission of the CA norepinephrine (NE) or the IA serotonin (5-hydroxytryptamine, 5-HT) respectively. Until recently, all drugs used to treat depression appeared to enhance neurotransmission in one or both of these systems, which was used to explain their antidepressant actions (Gelenberg and Klerman, 1978). In fact, it was this action of antidepressants that gave rise to the models of depression. Another way to increase brain levels of NE and 5-HT, and potentially to increase presynaptic activity, would be the systemic administration of the precursors of the neurotransmitters, an approach something like organic gardening in the brain. For this purpose, the 5-HT precursors tryptophan and 5-hydroxtryptophan (5-HTP), and the NE precursors tyrosine and dihydroxyphenylalanine (DOPA), have been administered to depressed patients. This paper reviews some of the theoretical background and clinical experience with the precursor strategy, focusing primarily on work with L-tyrosine. All four precursors as possible antidepressants have been recently reviewed (Gelenberg, 1982).
 ...
PMID:Tyrosine for the treatment of depression. 644 84

The investigation of catecholamine (CA) metabolism in animals subjected to various types of stress (different pain syndromes; cranial trauma; immobilization; cooling) and physical exercise shows considerable similarity among species in the sequence of changes, leading from the activation to the depletion of the sympathoadrenal system. The changes caused by physical exercise tend to be more pronounced in individuals with a genetic predisposition to greater stress responses. Stress adaption, induced by special training or by long-duration exposure to hypoxia, can substantially prevent the changes caused by physical exercise. Trained rats at rest show accelerated CA turnover, and after exercise, adaptive hypometabolic changes. Physical exercise causes both unspecific changes in CA metabolism, similar to those seen after other types of stress, and more specific ones, i.e., suppression of tissue CA synthesis and nonresponsiveness to exogenous L-tyrosine or L-DOPA. Adrenal CA synthesis could be restored in such animals by treatment with glucocorticoids and cyclic-AMP (c-AMP). The depression of CA synthesis after hard physical activity may be a mechanism for protecting the body from the injurious effect of the excessive CA release that would occur under stress.
 ...
PMID:Effects of physical activity and other types of stress on catecholamine metabolism in various animal species. 654 Dec 42

The present study using 8-day-old White Leghorn male chicks, was made to determine whether retarded growth of chicks fed a tyrosine excess (Tx) diet ad lib was due to the depression in feed intake or the reduced efficiency of feed utilization. A Tx diet was prepared by supplementing a 20% crude protein basal diet with 5% L-tyrosine. The levels of feed intake prepared for 10 days were as follows: 160 (corresponding to the amounts of the basal diet the chick would consume ad lib), 140, 120 (corresponding to the amounts of the Tx diet the chick would consume ad lib), 100, and 80 g per bird. Body weight gain, gain:feed ratio, and energy retention rate of chicks fed the basal or Tx diet decreased proportionally as the level of feed intake was decreased. The addition of Tx to the basal diet significantly reduced the body weight gain, gain:feed ratio, metabolizable energy (ME) value, and nitrogen and energy retention rates at all levels of feed intake. Body composition was not significantly affected by the addition of Tx to the basal diet at all levels of feed intake. The plasma free tyrosine concentration was markedly increased by the addition of Tx to the basal diet and also with increments in feed intake. Dietary Tx per se had a decreasing effect on body weight gain, efficiencies of dietary nitrogen, energy utilization, and ME value. The growth retardation of chicks fed a Tx diet ad lib was due to the combined effects of the depression in feed intake and the reduced efficiency of feed utilization.
 ...
PMID:Effects of dietary excess tyrosine and level of feed intake on nitrogen and energy utilization in chicks. 716 21

The respiratory rhythm generator (RRG) is modulated by several endogenous substances, including acetylcholine (ACh) and noradrenaline (NA) that interact in several modulatory processes. To know whether ACh and NA interacted to modulate the RRG activity, we used medullary "en bloc" and slice preparations from neonatal mice where the RRG has been shown to receive a facilitatory modulation from A1/C1 neurons, via a continuous release of endogenous NA and activation of alpha2 adrenoceptors. Applying ACh at 25 microM activated the RRG but ACh had no effects at 50 microM. Applying the ACh receptor agonists nicotine and muscarine facilitated and depressed the RRG, respectively. After yohimbine pre-treatment that blocked the alpha2 facilitation, the nicotinic facilitation was not altered, the muscarinic depression was reversed and ACh 50 microM significantly facilitated the RRG. After L-tyrosine pre-treatment that potentiated the alpha2 facilitation, the muscarinic depression was enhanced. Thus, ACh regulates the RRG activity via nicotinic and muscarinic receptors, the muscarinic receptors interacting with alpha2 adrenoceptors.
 ...
PMID:Muscarinic receptors and alpha2-adrenoceptors interact to modulate the respiratory rhythm in mouse neonates. 1726 95


1 2 Next >>