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)

The effects of treatment with and withdrawal from lithium (Li, 2 mmol/kg) on central catecholamine systems in rat brain were investigated. Synthetic parameters were found to be unchanged after treatment, but abrupt withdrawal resulted in enhanced activity of tyrosine hydroxylase. Noradrenaline levels in most brain regions examined were depressed following both short- and long-term Li administration, with a further decrease in content in the pons but enhanced cortical levels on withdrawal. Li administration resulted in elevated 3,4-dihydroxyphenylacetic acid levels, whereas withdrawal caused an enhancement of homovanillic acid content and depression of 3-methoxy-4-hydroxyphenyl glycol levels. It appears that the changes in central catecholamine systems are qualitatively the same following both short- and long-term Li treatment, as are the consequences of abrupt Li withdrawal. It is suggested that Li administration results in a disruption of catecholamine storage processes, while withdrawal from Li does not result in a simple return towards normal states.
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PMID:Comparison of the changes in central catecholamine systems following short- and long-term lithium treatment and the consequences of lithium withdrawal. 615 62

Recent prospective studies suggest that thyroid state plays a role in affective disorders. A lack of thyroid hormones can lower the threshold for depression; an excess can contribute to a state of tense dysphoria. Thyroid function in some persons also appears to influence the course of affective disorders. Adequate mobilization of thyroid hormones favors recovery from depression; excess mobilization increases the risk of mania in vulnerable individuals. Although other mechanisms may be involved, evidence suggests that the modulation by thyroid hormones of the beta-adrenergic receptor response to catecholamines may contribute to these effects. Norepinephrine stimulates such receptors; thyroid hormones increase their ability to receive stimulation. The plausibility of such interactions between catecholamines and thyroid hormones occurring in the CNS is strengthened by their common origin in the amino acid tyrosine and by their synergism in many metabolic processes.
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PMID:A hypothesis of thyroid-catecholamine-receptor interaction. Its relevance to affective illness. 625 96

1 Effects of noradrenaline or isoprenaline on the membrane and contractile properties of the smooth muscle cell, or on the excitatory neuro-effector transmission in the dog trachea, in vitro, were observed by use of microelectrodes and double sucrose gap methods.2 Noradrenaline (<5 x 10(-6) M) or isoprenaline (<5 x 10(-7) M) modified neither the membrane potential nor the membrane resistance. Increased concentrations of noradrenaline (>5 x 10(-5) M) depolarized and isoprenaline (>5 x 10(-7) M) hyperpolarized the membrane, and these actions were suppressed by phentolamine and propranolol respectively. Both catecholamines reduced the membrane resistance.3 Noradrenaline (5 x 10(-6) M) or isoprenaline (5 x 10(-7) M) reduced the resting tension, raised the mechanical threshold required to produce the contraction and suppressed the amplitude of phasic contractions evoked by electrical depolarization of the membrane.4 The action potential evoked by an outward current pulse in the presence of tetraethylammonium (TEA) was not affected by 5 x 10(-6) M isoprenaline, while the mechanical response was markedly suppressed.5 The excitatory junction potential (e.j.p.) evoked by electrical field stimulation was blocked by atropine. Noradrenaline (5 x 10(-7) M) or isoprenaline (5 x 10(-8) M) suppressed the amplitude of e.j.p. with no change in the membrane potential or input membrane resistance. Depression in the amplitude of e.j.ps produced by noradrenaline or isoprenaline reduced the amplitude of phasic contractions evoked by e.j.ps.6 These inhibitory actions of the catecholamines on mechanical responses and on e.j.ps were suppressed by pretreatment with propranolol (4 x 10(-6) M).7 Dog tracheal smooth muscles are innervated by cholinergic excitatory and adrenergic inhibitory systems. Electrical field stimulation produced excitation of both cholinergic and adrenergic nerve fibres, and propranolol (4 x 10(-6) M) enhanced the amplitude of e.j.p. generated by excitation of cholinergic nerves when repetitive stimulation (10 stimuli at 20 Hz) was used, but not the amplitude of the e.j.p. evoked by a single stimulus.8 5-Hydroxytryptamine (6 x 10(-6) M) produced a tonic contracture of the dog trachea. After pretreatment with atropine (4 x 10(-6) M), field stimulation (50 mus in duration and repetitive stimuli at 20 Hz) induced reversal of the contracture induced by 5-hydroxytryptamine and this was abolished by propranolol (5 x 10(-6) M).9 These results indicate that endogenous or exogenous catecholamines, in relatively low concentrations, predominantly activate beta-adrenoceptors in the pre- and post-junctional membrane in the dog trachea, and induce muscle relaxation.
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PMID:Dual effects of catecholamines on pre- and post-junctional membranes in the dog trachea. 627 18

Responses of the smooth muscle membrane of the rabbit bladder to intramuscular nerve stimulation were investigated by the micro-electrode and double sucrose-gap methods. The cell generated regular spontaneous action potentials. Acetylcholine produced a maintained increase in the frequency and ATP a transient increase. Noradrenaline only increased the frequency at very high concentrations. Application of short current pulses (50 microseconds) produced an initial excitatory junction potential (e.j.p.) with a superimposed spike, followed by a late depolarization. On some occasions, hyperpolarization of the membrane appeared between initial e.j.p. and the late depolarization. All these responses were abolished by tetrodotoxin. The late depolarization was enhanced by pre-treatment with neostigmine and abolished by atropine. This means that the delayed depolarization is due to activation of the muscarinic receptor. When the late depolarization was abolished, the amplitude of hyperpolarization was enhanced. The e.j.p. and contraction were unaffected by guanethidine, phentolamine, methysergide, mepyramine, quinidine or theophylline. This means that the e.j.p. is not mediated by activation of adrenergic, tryptaminergic, histaminergic or purinergic receptors. ATP reduced the amplitude of the e.j.p. due to depolarization of the membrane and reduction in the membrane resistance. The amplitude of the e.j.p. was gradually reduced by repetitive stimulation (0.5-2.0 Hz). However, the rate of depression was unchanged in the presence of ATP. Dipyridamole did not change the electrical and mechanical responses to field stimulation. These results do not support the proposal that ATP is the non-cholinergic excitatory transmitter. Apamine and tetraethylammonium (TEA) suppressed the hyperpolarization produced by field stimulation but guanethidine did not inhibit the hyperpolarization. Therefore, the hyperpolarization is due to increased K conductance of the membrane but it is not possible to conclude whether this component is due to the inhibitory action of a neurotransmitter or solely to after hyperpolarization of the spike. It was concluded that the rabbit bladder receives both cholinergic and noncholinergic excitatory neurones.
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PMID:Electrical and mechanical activity recorded from rabbit urinary bladder in response to nerve stimulation. 630 43

An investigation has been made of the effects of noradrenaline on excitatory transmission at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse of the rat olfactory cortex slice by measuring the effects of bath-applied noradrenaline on the amplitudes and latencies of the field potentials evoked on LOT stimulation. Low concentrations of noradrenaline (0.1-5 microM) facilitate transmission whereas higher doses (20-250 microM) depress transmission. Both these effects were completely blocked by non-selective alpha- and beta-adrenoceptor antagonists, by 2-amino-5-phosphonovaleric acid (an antagonist of excitatory amino acid receptors of the N-methyl-D-aspartate type) and by the methylxanthine theophylline. The depressant effects of noradrenaline were mimicked by bath application of GABA or adenosine and specifically antagonized by bicuculline and picrotoxin. In parallel experiments, noradrenaline (100 microM) significantly increased the potassium-evoked release of endogenous aspartate, glutamate and GABA, proposed transmitters of the olfactory cortex, although the effect on GABA release was specifically antagonized by 2-amino-5-phosphonovaleric acid. Noradrenaline (100 microM) also significantly increased the potassium-evoked release of D-[3H]aspartate, an effect antagonized by a number of alpha- and beta-adrenoceptor antagonists. It is concluded that at low concentrations, noradrenaline facilitates transmission at the LOT-superficial pyramidal cell synapse by increasing excitatory amino acid neurotransmitter release. This effect is mediated by both alpha- and beta-adrenoceptors although the primary site of release is unknown. At higher concentrations of noradrenaline, the increased levels of excitatory transmitters release sufficient endogenous GABA (and possibly adenosine) to cause an overall depression of transmission. These conclusions are supported by the results of a series of experiments in which the effects of noradrenaline on stimulus input-evoked field potential output relationships were assessed. It is not possible to exclude additional direct effects of noradrenaline on membrane excitability.
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PMID:Excitatory and inhibitory effects of noradrenaline on synaptic transmission in the rat olfactory cortex slice. 632 21

The urinary excretion rates of norepinephrine were assayed in 26 patients diagnosed as major depressive disorders (primary, unipolar), before and after 14 days of treatment with the monoamine oxidase inhibitor Moclobemide (Ro 11-1163). A standardized 1-h urine collection procedure was used and norepinephrine was assayed by liquid chromatography with electrochemical detection. Norepinephrine was found significantly increased in depressed patients when compared with a control population. The psychotic patients showed the highest excretion rates although they were not significantly different from the endogenous (non-psychotic) group. Urinary norepinephrine output significantly decreased after 14 days of treatment with Moclobemide. This decrease was also marked in those patients that did not show any therapeutic effect. A clear antidepressant effect, shown by a significant decrease of the Hamilton Scale scores for depression, was apparent as early as the 7th day. Increased norepinephrine in melancholic patients was taken as a presumptive indication of altered sympathetic activity.
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PMID:High urinary norepinephrine excretion in major depressive disorders: effects of a new type of MAO inhibitor (Moclobemide, RO 11-1163). 651 93

Circular muscle strips of rat uterus were obtained in the morning on Days 21 and 22 of pregnancy, and on the first postpartum day. Changes in the effects of noradrenaline and isoprenaline due to pregnant stage and incubation period in vitro were investigated, taking the contractile response and membrane activity as indicators. Plateau potential was dominant in Day 21 and postpartum preparations, and spike potential on Day 22. Noradrenaline (3 X 10(-7), 10(-6) M) caused excitation in Day 21 and postpartum preparations, whereas it caused inhibition in Day 22 preparations during early exposure to Krebs solution. When contractile potentiation was caused, plateau potential was prolonged, and when contractile depression was caused the plateau potential was suppressed. By incubation in vitro with Krebs solution, a transformation of the effect of noradrenaline from excitation to inhibition was caused in Day 21 preparations, and from strong to weak inhibition in Day 22 preparations. Isoprenaline of 3 X 10(-10) M concentration markedly depressed the contractile response in Day 22 preparations, whereas 10(-8) M isoprenaline was not enough to suppress the spontaneous contractions in postpartum preparations.
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PMID:Changes in the adrenergic effects and membrane activity of the circular muscle of rat uterus during late pregnancy and postpartum. 672 67

Dichlorvos (O,O-dimethyl-2:2-dichlorovinyl phosphate) was administered IP (3 mg/kg) daily for 10 days to a group of albino rats. Open field behavior was significantly depressed below the mean of the control group. On day 7, ambulation was reduced to 24% of the mean but recovered to 60% on day 10. Similarly, rearing response was decreased on day 7 and showed a fast recovery on day 10 but the preening response further declined on day 10. Defecation, on the contrary, was suppressed to 0% on day 7 and showed complete recovery on day 10. Motor activity showed a significant depression and fine movements were reduced more than gross movements in the second phase. Dopamine was significantly decreased on days 5 and 7 but showed a 13% recovery in the brain stem on day 10. Norepinephrine was significantly reduced in the cerebral hemisphere while serotonin was decreased both in cerebral hemisphere and brain stem. Neither of thse two amines showed significant recovery on day 10. Interesting concordance of the open field behavioral changes with the levels of dopamine, norepinephrine, and serotonin in the various regions of the rat brain was noticeable and has been discussed.
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PMID:Effects of an organophosphate (dichlorvos) on open field behavior and locomotor activity: correlation with regional brain monoamine levels. 677 97

Noradrenaline levels and platelet and free serotonin concentrations were studied in depressed women in-patients (n=78) before and during amitriptyline (n=41) or lithium treatment (n=37). Pronounced monthly differences in platelet serotonin level have been shown in these subjects before treatment. In all clinical subgroups (neurotic, involutional, manic-depressive patients) a significant fall in platelet serotonin level was observed with amitriptyline medication while an increase was noted with lithium. No significant correlations between serotonin concentrations and clinical outcome were found. Amitriptyline treatment also produced a decrease in peripheral noradrenaline concentration in all subgroups, while an increase was observed with lithium. Some correlations between noradrenaline level and degree of depression were noted in patients treated with amitriptyline or lithium. A more extended analysis of blood amine levels could supply meaningful information on the peripheral action of antidepressive drugs on noradrenaline and serotonin concentrations in depression.
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PMID:Blood noradrenaline and 5-HT levels in depressed women during amitriptyline or lithium treatment. 681 45

Experiments were performed on isolated rat aorta and superior mesenteric artery in order to study the action of nifedipine on norepinephrine and K-depolarization-evoked contractions and transmembrane calcium fluxes. Concentration-dependent contractions were obtained with norepinephrine in physiological solution and with Ca++ in K-depolarizing solution. Nifedipine caused a concentration-dependent depression of the maximum response. When aorta was depolarized by 40 mM KCI (instead of usual 100 mM KCI concentration), high concentrations of Ca++ evoked a relaxation that was also blocked by nifedipine. The action of nifedipine has been examined on Ca influx and efflux in arteries stimulated by norepinephrine and K-depolarization. Norepinephrine-evoked Ca influx, but not Ca efflux, was reduced by nifedipine. Concentration inhibitory curves for Ca influx and contraction could be superimposed. K-depolarization-dependent Ca entry and Ca efflux were blocked by nifedipine at concentrations lower than those required to antagonize norepinephrine actions. The results suggest that the action of nifedipine on artery contractility can be related to blockade of calcium entry through channels opened during depolarization or receptor-response coupling.
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PMID:Actions of nifedipine on calcium fluxes and contraction in isolated rat arteries. 682 65


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