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

The monoamine hypothesis of depression originally proposed that depression is caused by a central deficiency of biogenic amines, and antidepressants were considered to work by correcting this deficiency. In the course of time, many studies have analysed monoamine metabolites in the urine, plasma and cerebrospinal fluid of patients and healthy controls under different conditions to test the hypothesis. These studies have failed to identify a robust metabolic disorder in depressive patients as a group. Certain subgroups of depressed patients have shown deviations in biogenic amine metabolism, the most consistent being reduced levels of the major serotonin and dopamine metabolites in the cerebrospinal fluid. Noradrenaline metabolism is influenced by the activity of the sympathetic nervous system, and thus increases in anxious patients regardless of their clinical diagnosis. On the other hand, development of new antidepressants and advances in receptor techniques, together with modern electrophysiologic and behavioural studies have given increasing support to a receptor supersensitivity hypothesis of depression, based on the evidence that antidepressants lead to subsensitivity or down regulation of beta-adrenoceptors, and adaptive changes may occur also in other receptor systems after two three weeks of antidepressant treatment. There is also growing evidence on the manifold interplay of noradrenergic and serotonergic systems in the mechanism of actions of effective antidepressant treatments, including the new and more selective therapeutic compounds. The rapidly increasing knowledge of the neurotransmitter receptors as well as of the relations between the different regulatory systems may lead to more specific intervention strategies in efforts to correct the biological malfunction in the heterogeneous collection of diseases classified as affective disorders.
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PMID:Monoaminergic mechanisms in affective disorders. 288 34

The 3H-noradrenaline pretreated, spontaneously beating, guinea-pig atrial preparation has been used as a model system to study the presynaptic and postsynaptic actions of selected drugs with stimulant (bemegride, pentylenetetrazol, picrotoxin, strychnine and 4-methyl-4-n-propylpiperidine hydrochloride), depressant (pentobarbitone, hydroxydione, trimethadione, 3-methyl-3-n-alkylglutarimide where alkyl = butyl, amyl or hexyl, 4-methyl-4-n-propylpiperidone-2 hydrochloride, chlordiazepoxide and chlorpromazine) or dual stimulant-depressant (3-methyl-3-n-propylglutarimide and 5-ethyl-5-(1,3-dimethylbutyl) barbiturate and its (+) and (-) enantiomers) actions in the central nervous system of the mouse. 3H-Noradrenaline efflux and force and rate of atrial contraction were used as parameters of atrial function. With the exception of strychnine, picrotoxin and 4-methyl-4-n-propylpiperidine hydrochloride, which appear to act by different central mechanisms, there is good correspondence between the actions of the test drugs on the force of atrial contraction and in the CNS of the mouse. Thus, stimulant drugs increase and depressant drugs decrease the force of atrial contraction, while dual stimulant-depressant drugs in low concentrations increase, and in higher concentrations, decrease the inotropic response. A similarly good correspondence generally exists between mouse and atrium with respect to the relative stimulant and depressant potencies of the test drugs, additive stimulation or depression for pairs of like-acting drugs and 'analepsis' and 'anticonvulsant activity' for drugs with opposed central actions. No such relationships were found using tritium efflux or the chronotropic response as parameters of atrial function. Thus, the guinea-pig atrial preparation appears to be a good model system in which to demonstrate the acute CNS actions and interactions of the majority of the test drugs. Their positive and negative inotropic effects on the atrium have been explained in terms of a membrane phase distribution hypothesis of drug action, and their ability to facilitate or impede, respectively, the movement of Ca2/ across the atrial sarcolemmal membrane. It is proposed that these drugs may act by similar mechanisms at responsive sites in the brainstem reticular formation and related areas in the mouse. These may be primarily excitatory noradrenergic synapses integrated functionally with presynaptic or independent inhibitory GABAergic terminals.
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PMID:The guinea-pig isolated atrium as a model system for the central actions of selected CNS stimulant and depressant drugs. Part 1: 3,3-Diakylglutarimide homologues and related drugs. 289 85

The effects of induction of anesthesia with diazepam and midazolam on baroreflex control of heart rate and on plasma levels of catecholamines were investigated in this study. Group 1 subjects (n = 10) received diazepam, 0.4 mg/kg. Group 2 subjects (n = 10) received midazolam, 0.3 mg/kg. Baroreflex function was assessed using a pressor test (phenylephrine). In addition, samples for subsequent determination of plasma norepinephrine and epinephrine levels and plasma diazepam or midazolam concentrations were collected before and 5, 10, and 15 min after intravenous drug administration. The pressor baroreflex slope declined significantly after diazepam or midazolam administration with the maximal changes (-45 and -43%, respectively) observed when plasma diazepam or midazolam concentrations were the highest. Norepinephrine plasma concentrations decreased at each measurement with both drugs. In contrast, epinephrine concentration decreased only after midazolam. The authors conclude that diazepam or midazolam used for induction of anesthesia results in a transient depression of baroreflex function and a sustained decrease of sympathetic tone. This study also indicates that the depression of arterial baroreflex heart rate responses under diazepam or midazolam anesthesia are less pronounced than the depression of baroreflex responses reported by other investigators with potent inhalational anesthetics. However, this disruptive effect of diazepam and midazolam on sympathetic control of circulation might induce a limited ability to compensate for hemodynamic alterations related to hypovolemia.
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PMID:Effects of diazepam and midazolam on baroreflex control of heart rate and on sympathetic activity in humans. 293 50

We have investigated the type of purine receptor in the guinea-pig olfactory cortex, using pial surfaces slices maintained in vitro. Adenosine (0.1 to 100 mumol/l) bath applied in the presence of the uptake inhibitor nitrobenzylthioinosine, depressed the evoked potentials in a dose related fashion. Synthetic and uptake resistant adenosine analogues had the same effect as adenosine and the order of potency of these was: 5'-N-ethylcarboxamide adenosine greater than L-N6-phenylisopropyl adenosine (L-PIA) = N6-cyclohexyladenosine = 2-chloroadenosine greater than adenosine greater than D-N6-phenylisopropyladenosine (D-PIA). The D-stereoisomer of PIA was 45 times less potent than L-PIA. The methylxanthine compounds 8-phenyltheophylline (3 mumol/l) and 3-isobutyl-1-methylxanthine (50 mumol/l) antagonised the depression produced by L-PIA. Rolipram, a phosphodiesterase inhibitor, in concentrations up to 100 mumol/l had no effect on the evoked potentials or on adenosine action. Forskolin, a cAMP stimulant, slightly increased the amplitude of the evoked potential, and partly reversed the depressant effect of adenosine. Noradrenaline had no effect either alone or in the presence of adenosine. The results of these experiments indicate the existence of A1 subtype adenosine receptors in the guinea pig olfactory cortex probably linked to a depression of intracellular cAMP.
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PMID:Adenosine-induced depression of synaptic transmission in the isolated olfactory cortex: receptor identification. 298 40

Noradrenaline (NA) synthesis in rat hippocampal synaptosomes is increased by calcium ionophore, A23187, in the presence of calcium. Activation of presynaptic muscarinic, gamma-aminobutyric acidB (GABAB) and alpha 2-adrenergic receptors causes inhibition of the ionophore-stimulated synthesis. The results suggest that different mechanisms mediate the depression by presynaptic receptors of NA release and NA synthesis.
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PMID:Stimulation of noradrenaline synthesis by the calcium ionophore A23187 and its modulation by presynaptic receptors. 300 24

The central biochemical pathology of anorexia and the natural aging of the brain is similar. Biochemical models for drug withdrawal and depression may also assist in understanding geriatric anorexia. Norepinephrine, corticotropin releasing factor and beta-endorphin may key neurotransmitters in all of these conditions.
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PMID:Drug abuse and depression: possible models for geriatric anorexia. 326 10

In 35 initially normotensive patients with chronic glomerulonephritis and lupus nephritis (including 27 patients with nephrotic syndrome; NS), blood pressure (BP), urinary sodium excretion, plasma renin activity (PRA), plasma aldosterone level (PA), urinary aldosterone excretion (Au and blood volume were measured before and during prednisolone treatment. In 7 patients (all with NS) steroid-induced hypertension has developed. The patients prone to develop hypertension were hypervolemic nephrotics with initial depression of PRA, PA, Au, and severe sodium retention. In these patients prednisolone did not produce diuresis of natriuresis nor did it decrease proteinuria. In normo- and hypovolemic patients prednisolone produced significant diuresis and natriuresis and failed to induce hypertension. Thus, two types of response to prednisolone could be observed in patients with NS.
Nephron 1988
PMID:Steroid-induced hypertension in patients with nephrotic syndrome. 328 84

The effect of local sympathetic denervation on immune responses of submaxillary lymph nodes (SmLN) of mice was examined in animals subjected to unilateral superior cervical ganglionectomy (SCGx). Norepinephrine (NE) content in ipsilateral SmLN decreased by 90% 7-20 days after SCGx, while bilateral SCGx resulted in a 91% decrease of SmLN NE content. SmLN of mice subjected to unilateral SCGx exhibited greater plaque-forming cell (PFC) response than the innervated contralateral SmLN, when challenged i.d. or i.p. with sheep red blood cells (SRBC) 10-20 days after surgery. In mice challenged with SRBC at an early phase of sympathetic nerve paralysis (i.e., 2 h after SCGx), PFC response was already increased in the ipsilateral SmLN whereas during the anterograde degeneration of nerve endings (6-24 h after SCGx) an impending depression of PFC number was observed. Contact hypersensitivity and allogeneic delayed-type reactions were also enhanced in the ear ipsilateral to SCGx. Primed SmLN cells of nodes located ipsilaterally to SCGx, when injected to (BALB/c x C57BL/6) F1, resulted in significantly higher spleen index than similarly treated, contralateral SmLN. In contrast, mitogenic stimulation under various experimental protocols failed to reveal significant differences between proliferation of cell populations obtained from ipsilateral and contralateral SmLN of unilaterally SCGx mice. SmLN of mice parasympathetically decentralized by unilateral sections of the chorda tympani-lingual nerve trunk showed lower PFC response than the innervated contralateral SmLN, when challenged with SRBC 8-28 days after surgery. These results suggest a regulatory function of the autonomic nervous system in immune reaction.
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PMID:Autonomic nervous system regulation of murine immune responses as assessed by local surgical sympathetic and parasympathetic denervation. 333 31

Two cases of childhood nephrotic syndrom (NS) were diagnosed in September 1981 and February 1982, respectively. The patients were first cousins. There was no other family history of renal disease. Five months after onset of nephrosis in 1 patient and 1 month after onset of nephrosis in the other both had an intercurrent measles infection and the NS rapidly went into spontaneous remission. However, relapses occurred 3 and 7 months later. At that time both patients were started on steriod treatment and obtained remission. Unfortunately, both relapsed again 14 months later. Kidney biopsies were performed, the pathologic findings demonstrated that both were mild mesangial proliferative glomerulonephritis. The mononuclear cell subsets and lymphoproliferative responses were studied during the acute measles infection, 4 weeks later, in remission and relapse of NS. The mononuclear cell subsets and lymphoproliferative response in medium containing autologous serum with complement were decreased during the acute measles infection. Both patients had an increase of OKT8 cells and Leu-7 cells in relapse and a decrease in remission. Taken together, natural measles infection caused a prolonged depression of cell-mediated immunity, T cell subset and induced a temporary remission of steroid-sensitive NS.
Nephron 1986
PMID:Histopathological and immunological studies in spontaneous remission of nephrotic syndrome after intercurrent measles infection. 348 7

A quantitative, noninvasive method of assessing autonomic control, based on the spectral analysis of beat-to-beat fluctuations in heart rate (HR), was applied to patients with chronic renal failure (RF). Since the power spectrum of HR fluctuations measures the dynamic nervous control of HR, it can be used to quantitate a normal control system as opposed to a disturbed or depressed system. Indeed, in RF patients, a strong reduction in the HR power spectrum was observed in all frequency ranges, both sympathetically and parasympathetically mediated. A similar depression in autonomic control was demonstrated in patients on hemodialysis or peritoneal dialysis. RF patients not yet undergoing dialysis show a lesser degree of depression. Spectral analysis of HR fluctuations in RF patients makes it possible to quantitate autonomic dysfunction and to reliably measure its development as a function of time, and requires only a 10-min standard electrocardiogram recording.
Nephron 1987
PMID:Spectral analysis of fluctuations in heart rate: an objective evaluation of autonomic nervous control in chronic renal failure. 357 69


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