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 possibility that zinc (Zn2+) induces giant depolarizing potentials (GDPs) by blocking pre- and postsynaptic gamma-aminobutyric acidB (GABAB) receptors in area CA1 of rat hippocampal slices was investigated. Monosynaptic GABAA receptor-mediated fast and GABAB receptor-mediated late inhibitory postsynaptic potentials (IPSPs) were evoked in the presence of the excitatory amino acid (EAA) receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and D,L-amino-5-phosphonovalerate (APV). Addition of Zn2+ (0.3 mM) resulted in the appearance of long-lasting GDPs which obscured monosynaptic late IPSPs. The GABAA receptor antagonist bicuculline methiodide (BMI; 30 microM) blocked fast monosynaptic IPSPs and GDPs, revealing a monosynaptic late IPSP that was prolonged in the presence of Zn2+ and blocked by the GABAB receptor antagonist CGP 35,348 (100 microM). The selective GABAB receptor agonist baclofen (10 microM) depressed monosynaptic IPSPs and population excitatory postsynaptic potentials (pEPSPs) by acting at presynaptic GABAB receptors. Depression of synaptic potentials by baclofen was unaffected by Zn2+. These results suggest that induction of GDPs in area CA1 does not result from an action of Zn2+ at GABAB receptors. We suggest instead that Zn2+ induces GDPs by inducing synchronized discharge of GABAergic interneurons.
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PMID:Induction of giant depolarizing potentials by zinc in area CA1 of the rat hippocampus does not result from block of GABAB receptors. 135 30

Plasma taurine and serine decrease following trauma and in severe inflammatory disease. These changes may signify an increase in requirements for sulfur amino acids. We previously demonstrated that cysteine supplementation can restore the impaired ability of rats fed an 8% casein diet to increase hepatic zinc, glutathione (GSH) and protein concentrations in response to tumor necrosis factor alpha (TNF alpha). Here we examined whether serine or taurine produces a similar effect, because serine provides the carbon skeleton of cysteine and taurine is its major metabolite. After 7 d of receiving either a 20% casein diet supplemented with cysteine or an 8% casein diet supplemented with alanine, serine or taurine, rats received an intraperitoneal injection of human TNF alpha. Tumor necrosis factor caused no change in hepatic GSH but resulted in a lower GSH concentration in lung in rats fed the alanine-supplemented diet. Neither taurine nor serine increased liver GSH relative to that in rats fed alanine, but the depression in lung due to TNF injection was lessened. The absolute increase in ceruloplasmin in response to TNF was enhanced in rats fed the alanine-supplemented diet relative to those fed the 20% casein diet. Serine normalized this response. This observation--the effects of taurine and serine on lung GSH and a significant negative correlation between ceruloplasmin and liver and lung GSH concentration in rats fed TNF--suggests that supplemental serine and taurine may improve antioxidant defenses when dietary supplies of cysteine are low but do not influence cysteine availability for a normal response to TNF.
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PMID:Taurine and serine supplementation modulates the metabolic response to tumor necrosis factor alpha in rats fed a low protein diet. 137 44

1. The M-like current IK(M,ng) in differentiated NG108-15 mouse neuroblastoma x rat glioma hybrid cells has been studied using tight-seal, whole-cell patch-clamp recording. 2. When calculated from steady-state current-voltage curves, the conductance underlying IK(M,ng) showed a Boltzmann dependence on voltage with half-activation voltage Vo = -44 mV (in 3 mM [K+]) and slope factor (a) = 8.1 mV/e-fold increase in conductance. In 12 mM [K+] Vo = -38 mV and a = 6.9 mV. The deactivation reciprocal time constant accelerated with hyperpolarization with slope factor 17 mV/e-fold voltage change. 3. The reversal potential for deactivation tail currents varied with external [K+] as if PNa/PK were 0.005. 4. Steady-state current was increased on removing external Ca2+. In the presence of external Ca2+, reactivation of IK(M, ng) after a hyperpolarizing step was delayed. This delay was preceded by an inward Ca2+ current, and coincided with an increase in intracellular [Ca2+] as measured with Indo-1 fluorescence. Elevation of intracellular [Ca2+] with caffeine also reduced IK(M, ng). 5. IK(M, ng) was inhibited by external divalent cations in decreasing order of potency (mM IC50 in parentheses): Zn2+ (0.011) greater than Cu2+ (0.018) greater than Cd2+ (0.070) greater than Ni2+ (0.44) greater than Ba2+ (0.47) greater than Fe2+ (0.69) greater than Mn2+ (0.86) greater than Co2+ (0.92) greater than Ca2+ (5.6) greater than Mg2+ (16) greater than Sr2+ (33). This was not secondary to inhibition of ICa since: (i) inhibition persisted in Ca(2+)-free solution; (ii) La3+ did not inhibit IK(M, ng) at concentrations which inhibited ICa; and (iii) organic Ca2+ channel blockers were ineffective. Inhibition comprised both depression of the maximum conductance and a positive shift of the activation curve. Addition of Ca2+ (10 microM free [Ca2+]) or Ba2+ (1 mM total [Ba2+]) to the pipette solution did not significantly change IK(M, ng). 6. IK(M, ng) was reduced by 9-amino-1,2,3,4-tetrahydroacridine (IC50 8 microM) and quinine (30 microM) but was insensitive to tetraethylammonium (IC50 greater than 30 mM), 4-aminopyridine (greater than 10 mM), apamin (greater than 3 microM) or dendrotoxin (greater than 100 nM). 7. IK(M, ng) was inhibited by bradykinin (1-10 microM) or angiotensin II (1-10 microM), but not by the following other receptor agonists: acetylcholine (10 mM), muscarine (10 microM), noradrenaline (100 microM), adrenaline (100 microM), dopamine (100 microM), histamine (100 microM), 5-hydroxytryptamine (10 microM), Met-enkephalin (1 microM), glycine (100 microM), gamma-aminobutyric acid (100 microM) or baclofen (500 microM).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Kinetic and pharmacological properties of the M-current in rodent neuroblastoma x glioma hybrid cells. 140 9

This study was conducted to determine the zinc status and assess relationship between serum zinc and in vivo cell mediated immunity (CMI) in patients with rheumatic heart disease (RHD). The study comprised 22 patients with active rheumatic heart disease (ARHD), 15 patients with chronic rheumatic heart disease without activity (CRHD) (selection based on Jone's Criteria--Revised), and 15 age and sex matched healthy control. Zinc estimation was done by atomic absorption spectrophotometer. To assess CMI in vivo, phytohaemagglutinin skin test and skin window test were done. Serum zinc and in vivo CMI in patients with ARHD and CRHD compared with controls. Mean serum zinc was significantly decreased in patients with ARHD and CRHD, more pronounced in the former (P less than 0.001); and mean 24 h urinary zinc was significantly increased in patients with ARHD (P less than 0.001) as compared to controls. A significant depression in CMI in vivo was observed in patients with ARHD and CRHD (P less than 0.001). A significant positive correlation was seen among serum zinc and markers of in vivo CMI (P less than 0.001). In conclusion, depletion of zinc, observed in RHD, probably causes immune alterations and suggest role of zinc in immunopathogenesis of RHD. Zinc supplementation may alter the course of rheumatic fever and RHD.
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PMID:A correlative study of serum zinc and in vivo cell mediated immune status in rheumatic heart disease. 152 10

1. Decreased febrile responses to interleukin-1 and endotoxin have been noted in a number of species with ageing. 2. The present study extends these observations by examining the pyrogenic response to intravenous recombinant human tumour necrosis factor-alpha (50 micrograms/kg) using conscious rats aged 7,20 and 80 weeks. 3. The febrile response decreased in magnitude and duration with age. Fevers of 0.9 degree C and of 5 h duration were observed in the youngest rats, whereas those aged 80 weeks were afebrile. The depression in serum zinc level and the elevation in liver zinc level, which occurred 7 h after injection, were unaffected by age. 4. The mechanism of the reduced pyrogenic response was examined by assessing prostaglandin E2 production in vitro from hypothalami of rats, aged 10 and 24 weeks, in response to Escherichia coli endotoxin and tumour necrosis factor. 5. Whereas the production of prostaglandin E2 increased by 47% and 52%, respectively, in hypothalami from 10-week-old rats, no response to either pyrogen was obtained in tissue from rats aged 24 weeks. 6. Maturity brings about a decreased responsiveness of hypothalamic prostaglandin E2 production to pyrogens, which may explain the decreased febrile responses observed.
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PMID:Effect of age on hypothalamic prostaglandin E2 production and fever in response to tumour necrosis factor (cachectin) and endotoxin in rats. 165 31

Urinary zinc excretion normally plays a minor role in zinc homeostasis; however, urinary zinc excretion is markedly elevated after trauma or surgery, and mechanism(s) for this zinc loss are poorly defined. In this study we evaluated multiple potential mechanisms for increased urinary zinc excretion in patients with thermal injury. We documented that patients with severe thermal injury had markedly elevated urinary zinc excretion. Above 20% total body surface area burn, however, the severity of thermal injury did not correlate with urinary zinc excretion. Serum zinc concentrations were depressed on initial evaluation and gradually increased during the hospital course, whereas peak urinary zinc excretion occurred 2 to 5 weeks after injury. Thus the depression in serum zinc concentration did not temporally relate to the observed pattern of hyperzincuria. Increased urinary zinc excretion also did not temporally relate to urinary excretion of the amino acids cysteine and histidine (both of which tightly bind zinc) nor to urinary 3-methylhistidine excretion, a marker of muscle breakdown. Urinary amylase excretion, a marker of renal tubular dysfunction, did follow the pattern of urinary zinc loss to some extent, although this correlation was not perfect. Increased oral intake of zinc via zinc supplements resulted in significantly increased urinary zinc excretion. Patients receiving total parenteral nutrition (TPN) did not have significantly increased urinary zinc excretion when compared with people receiving their total nutrient intake by mouth.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased urinary zinc excretion after thermal injury. 174 2

The toxicity of Z-103 (catena-(S)-[mu-[N alpha-(3-aminopropionyl) histidinato(2-)-N1,N2,O:N tau]-zinc], CAS 107667-60-7) was evaluated in mice and rats after single administration. LD50 values in mice were 1269 mg/kg for males and 1331 mg/kg for females by the oral route, 220 mg/kg for males and 165 mg/kg for females by the intraperitoneal route, and 758 mg/kg for males and 874 mg/kg for females by the subcutaneous route. LD50 values in rats were 8441 mg/kg for males and 7375 mg/kg for females by the oral route, 405 mg/kg for males and 422 mg/kg for females by the intraperitoneal route and more than 5000 mg/kg for both sexes by the subcutaneous route. No sex differences were observed. A decrease in locomotor activity, ventral posture, crouching, hypothermia and respiratory depression were observed in both mice and rats as the main clinical signs. In addition to these changes, induration, swelling and crust formation were observed at the subcutaneous injection site.
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PMID:Single dose toxicity study on catena-(S)-[mu-[N alpha-(3-aminopropionyl) histidinato(2-)-N1,N2,O:N tau]-zinc] in mice and rats. 179 79

The study was undertaken to estimate plasma copper and zinc in thirty-five depressed patients. Two blood samples were drawn from each patient, one before starting treatment and the second after recovery from depression. The results were compared with the thirty-five normal healthy individuals. The mean plasma copper in controls, depressed patients and in patients after recovery were 106.82, 122.14 and 104.22 micrograms/dl, respectively. The copper levels in patients when depressed were significantly higher as compared to controls and after recovery from depression. The mean plasma zinc levels in controls, depressed patients and after recovery were 115.80, 107.62 and 125.68 micrograms/dl, respectively. No significant difference could be obtained between control and depressed patients. However, the values were significantly higher in recovered patients compared to patients with depression.
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PMID:Levels of copper and zinc in depression. 181 5

We reviewed the records of 42 patients with Wilson's disease participating in a zinc acetate treatment protocol and interviewed 17 of them. Five of the patients studied were asymptomatic. A significant number of symptomatic patients (64.8%) reported psychiatric symptoms at the time of initial presentation. These symptoms were severe enough to warrant psychiatric intervention in almost half of all symptomatic patients before the diagnosis of Wilson's disease was made. Personality changes, particularly irritability and aggression, were most commonly described (45.9%), followed by depression (27%). Cognitive changes, anxiety, psychosis, and catatonia, while less frequent, also occurred. These data underscore the need to include Wilson's disease in the differential diagnosis of psychiatric disorders.
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PMID:The psychiatric presentations of Wilson's disease. 149 90

The depression of immunity to various antigens in chronic uremia is a frequently encountered phenomenon. Zinc deficiency might well be an important factor in its genesis. The aim of this study was to investigate the role of zinc deficiency in this reduced immune response. Two groups of 7 patients on haemodialysis who had failed to respond with seroconversion to an earlier vaccination against hepatitis B were revaccinated. One group received zinc by the addition of zinc chloride to the dialysate. Before initiation of the study zinc in plasma and leucocytes was measured. No difference in plasma and leucocyte zinc was observed between the two groups. Zinc in leucocytes was lower in patients than in a group of healthy volunteers (61.5 pmol/10E6 cells +/- 4.6 versus 73.8 +/- 5.6, p less than 0.005). Plasma zinc showed no difference between patients and healthy volunteers. During zinc supplementation zinc in plasma rose in the patient group receiving zinc (10.4 mmol/L +/- 1.5 to 14.2 +/- 1.9, p less than 0.005). However, no rise in leucocyte zinc was seen. At the end of the trial seroconversion had occurred in 2 patients in each group. It is concluded that zinc supplementation in haemodialysis patients does not lead to the restoration of leucocyte zinc to normal levels. Neither did it lead to an enhanced antibody response in our population after revaccination of haemodialysis patients against hepatitis B.
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PMID:Effects of zinc supplementation on zinc status and immunity in haemodialysis patients. 182 9


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