UMLS:C0011570 - FACTA Search

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

1. An in vitro slice preparation of rat prefrontal cortex was used to analyse the responses of layer V pyramidal cells to electrical stimulation of layer II. We also studied the long-lasting modifications of synaptic efficacy following high-frequency stimulation of the same region. 2. Stable intracellular recordings were obtained from forty-three regular spiking pyramidal cells. The input resistance was 56 +/- 18 M omega (mean +/- S.D.) at a resting membrane potential of -71 +/- 4 mV. 3. At rest, a single stimulus of increasing strength evoked a monophasic, purely depolarizing postsynaptic potential (PSP) of increasing amplitude. In neurons recorded with potassium acetate-filled micropipettes, membrane depolarization disclosed an excitatory-inhibitory (EPSP-IPSP) sequence (onset latency of the EPSP, 3.6 +/- 0.6 ms). 4. Superfusion with the non-N-methyl-D-aspartate (NMDA) receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) reduced the EPSP and suppressed the IPSP. The small EPSP which remained was blocked by the NMDA receptor antagonist, D,L-2-amino-5-phosphonovalerate (APV). 5. In five cells, administration of 0.5 mumol l-1 bicuculline revealed a postsynaptic NMDA component in the evoked response as evidenced by its anomalous voltage dependence in the presence of Mg2+ and its sensitivity to APV. In these cells the latency of the APV-sensitive EPSP was the same as that of the APV-insensitive EPSP. 6. In six cells superfused with a high-Mg2+, low-Ca2+ artificial cerebrospinal fluid (ACSF) a small monosynaptic EPSP remained which had the same latency as the PSP recorded in control ACSF. 7. Patterned high-frequency stimulation (50-100 Hz) was applied to the afferents of twenty-eight neurons (twenty-three of them were recorded in the presence of bicuculline). During the train the membrane potential depolarized some 20 mV and each stimulus evoked a small PSP. The tetanic stimulation was followed by a short-term enhancement of the PSP amplitude and a slight increase in membrane input resistance. 8. Out of the twenty-eight cells, twenty-four showed long-lasting (over 30 min) modifications of the PSP. Long-term depression (LTD) of the evoked PSP was observed in fourteen cells and long-term potentiation (LTP) in ten cells. There was no significant change in the steady-state membrane properties and in the latency of the response. 9. In 64% of the cells that showed LTD and 70% of those that showed LTP of synaptic efficacy, the latency of the enhanced or depressed component of the PSP was the same as the control.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use-dependent changes in synaptic efficacy in rat prefrontal neurons in vitro. 221 2

A total of 180 crossbred, weanling pigs were assigned to five dietary treatment groups: 1) a basal corn-soybean meal diet formulated to current NRC recommendations, 2) basal + monosodium phosphate (2 x NRC P recommendations; P), 3) basal + alpha-tocopheryl acetate (220 IU/kg; E), 4) basal + sorbitol (1% of the diet; S) and 5) basal + PES. Dietary treatments were continued until market weight (104 kg). Blood samples were obtained at 3-wk intervals for analysis of serum alpha-tocopherol, P and total cholesterol. Liver and muscle (semimembranosus) samples were obtained at the end of the starter, grower and finisher phases for determination of total cholesterol concentration. The Ca:P imbalance produced by the high-phosphorus diets (P and PES) increased feed intake during the finisher phase. Dietary treatment did not consistently affect total serum cholesterol at any phase of growth. A transient 21.5% (P less than .05) depression of liver cholesterol concentration was observed in the PES-fed pigs at the end of the starter phase but was not apparent at market weight. A similar trend (nonsignificant) was noted for muscle cholesterol concentration. The present study suggests that the PES diet can decrease tissue cholesterol concentration during the nursery phase, but it remains uncertain whether this transient response is a function of age and(or) diet transition at weaning. Further research is necessary to determine whether this response can be translated to the finishing phase, and thereby reduce carcass cholesterol.
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PMID:Effect of vitamin E, phosphorus and sorbitol on growth performance and serum and tissue cholesterol concentrations in the pig. 225 1

According to the literature, Cyclosporine A (CsA) is said to suppress specifically the activity of T and B cells. A significant influence on phagocyte function has been neglected. However, aggravated courses of bacterial and fungal infections have been frequently reported under the treatment with CsA, suggesting that a latent depression of phagocytic activity may possibly occur under clinical circumstances. Therefore, this study set out to assess whether CsA can also change granulocyte function under therapy conditions or not. Thirty-seven patients, 3 months-10 years after kidney transplantation being under immunosuppressive treatment with CsA + Prednisolone (n = 25), Azathioprine + Prednisolone (n = 6) and under Prednisolone alone (n = 6) underwent the study. 18 healthy persons served as a normal control group. Granulocyte function was tested ex vivo by chemiluminescence (CL) after stimulation with phorbolmyristate acetate (PMA) and with zymosan (zym) activated autologous or pool-serum. The obtained data were correlated to corresponding serum or plasma levels of CsA, human leukocyte elastase (HLE) and neopterin. Comparing the three therapy groups with the healthy control and with each other no differences could be seen in median CL values; but there was a significant (p = 0.05) negative correlation between CsA blood levels and maximum CL values of PMN. Such inhibition of CL could be calculated for zym but not for PMA stimulated PMN; suggesting that the CsA mediated inhibition of granulocyte function may be only partial and restricted to phagocytosis. In addition, a positive correlation between serum levels of human leukocyte elastase (HLE) and neopterin could be found. This indicates a simultaneous influence of CsA on both PMN and macrophages.
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PMID:Latent inhibition of granulocyte function by cyclosporine A. 227 42

The role of protein kinases in renal noradrenergic stimulation was examined using sphingosine, 1-(5-isoquinolinylsulfonyl)-2-methyl-piperizine (H7), using sphingosine, 1-(5-isoquinolinylsulfonyl)-2-methyl-piperizine (H7), or staurosporine to inhibit the responses to norepinephrine (NE, 60 nM) in isolated perfused rat kidneys. Sphingosine (20 mumol/L) increased the noradrenergic vasoconstrictor response. H7 (10 mumol/L) partially blocked the immediate vasoconstrictor response and completely inhibited it after 2 min without altering the antinatriuretic and antilithuretic responses. H7 also blocked the increase in free water produced by NE, which is consistent with the inhibition of protein kinase A linked to beta-adrenergic stimulation. Staurosporine (10 nmol/L) partially inhibited noradrenergic vasoconstriction and antinatriuresis, and it completely blocked the depression of gluconeogenic responses to NE in pyruvate-perfused kidneys. To examine the role of diacylglycerol and protein kinase C in the renal responses to NE, we used oleoyl-acetyl-glycerol (OAG, 50-100 microM) or phorbol-12-myristyl-13-acetate (TPA, 5-50 nM). TPA slowly vasoconstricted the kidney and reduced GFR and fractional Na+, Li+, and free water excretion. Amiloride (1 mM) prevented the TPA responses. OAG mimicked the effects of TPA except that vasoconstriction occurred more rapidly and was brief. Both TPA and OAG acted like alpha 1-adrenergic agonists. These results indicate that diaclyglycerol and protein kinase are involved in the prolonged effects of NE on vasoconstriction. GFR, and proximal tubular reabsorption.
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PMID:Diacylglycerol and protein kinase mediated noradrenergic responses in perfused rat kidneys. 239 Jul 42

Continuous, non-invasive measurement of arterial oxygen saturation (SaO2) during haemodialysis was performed in 18 patients with chronic renal failure. They were dialyzed three times for 2 1/2-3 1/2 h weekly using a capillary polysulfone (F60) or a cuprophane (D2) filter. The total number of O2 saturation curves analyzed was 48. The whole group showed a significant mean decline in SaO2 by 1.9% as compared with predialysis values. In 7 patients with three or more recordings, the significant mean decline in SaO2 was 1.5-4.2% and occurred within 15-60 min after onset of haemodialysis. Evaluation of SaO2 during episodes of severe depression of blood pressure was not possible due to loss of the signal as a consequence of peripheral vasoconstriction. Changes in SaO2 which occurred without any clinical signs or symptoms included very short episodes of depression of SaO2 by 3-22%; a decrease in SaO2 by 3-6% occurring towards the end of the treatment and followed by depressed values for a period of 20-60 min; episodes of marked instability of SaO2 values with differences of up to 10%, lasting 20-60 min and occurring towards the end of the treatment. Application of cuprophane instead of polysulfone filter membranes, first use and reuse of dialyzers, and microemboli blood filters were not found to influence the changes in SaO2. There was a significant difference in the initial decrease in SaO2 during acetate as compared with bicarbonate dialysis.
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PMID:Continuous pulse-oxymetry during haemodialysis. 239 88

Phosphatidylserine (PS) is a necessary cofactor for protein kinase C (PKC) activation, and changes in the synthesis of PS have been shown to participate in the mechanism(s) involved in the transmembrane signaling of interleukin 1 (IL-1). In view of the age-associated defects in T-cell functions, in the present study we have addressed the question of whether an in vivo treatment with PS might interfere with such processes. Furthermore, the effect of an in vitro treatment with PS in human peripheral blood monocytes (PBMC) or splenocytes activated with a lectin mitogen, on the expression of IL-2 receptor, was assessed. While the process of ageing was accompanied by a marked decline of humoral response monitored by anti-BSA antibodies (of the IgG class) production, following immunization with BSA in complete Freund adjuvant, chronic treatment with PS (50 mg/kg, in drinking water), reversed this effect, raising specific antibody titers to levels practically indistinguishable from those measured in young animals. Pharmacological depression of humoral immune response induced by a treatment of adult animals with dexamethasone was similarly reversed by a chronic treatment with PS. While only a pharmacological concentration (10(-5) M) of PS significantly increased IL-2 receptor expression in activated human PBMC, simultaneous treatment of PBMC with inactive doses of PS and the pharmacological activator of PKC (phorbol myristate acetate, PMA, 10(-8) M) resulted in a synergistic stimulation of Tac+ cells. Furthermore, in cultures of rat splenocytes PS (10(-6) M) significantly stimulated the expression of IL-2 receptor, and concomitant addition of PS (10(-7) M) to Con A-stimulated splenocytes produced a significant potentiation of IL-2 receptor induction. The present results indicate that in vivo treatment of ageing animals with the specific phospholipid PS is able to reverse the physiological decline of the humoral immune response induced by the ageing process. Moreover, treatment of young rats with PS reversed the pharmacological associated depression of specific antibody production. The in vitro effects of the phospholipid on human PBMC and rat splenocytes might suggest that PS is implicated in T-cell activation through its action on IL-2 receptor.
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PMID:Phosphatidylserine counteracts physiological and pharmacological suppression of humoral immune response. 239 81

Nine patients with psoriasis vulgaris were treated for 12 weeks with somatostatin analog, octreotide acetate (SMS 201-995) 50 or 100 micrograms by subcutaneous injection every 12 hours. The purposes of the study were to determine: (1) levels of insulin, glucose, glucagon, pancreatic polypeptide (PP), and SMS 201-995 after a subcutaneous injection of SMS 201-995 and ingestion of a standardized meal; (2) nocturnal (0200 h) thyroid stimulating hormone (TSH) levels before, during, and after treatment; and (3) the pharmacokinetics of SMS 201-995. Insulin peaks at 30 minutes were blunted from 65.8 +/- 11.0 mu U/mL without treatment to 26.7 +/- 8.6 mu U/mL and 7.7 +/- 2.0 mu U/mL after the 50- and 100-micrograms doses, respectively. Glucagon levels remained constant during the meal and were not affected by the 50-micrograms dose. Mean glucose levels were significantly elevated during insulin suppression. PP was also rapidly suppressed by SMS 201-995 and remained so for 4 hours after the injection. Nocturnal TSH was blunted after 12 weeks of treatment (P less than or equal to .05). T4 and T3 resin uptake showed no depression, and patients remained clinically euthyroid. The plasma peak of SMS 210-995 occurred 30 minutes postinjection and half-life was longer than 2 hours. After chronic administration of SMS 201-995, insulin was suppressed with resultant mild carbohydrate intolerance that persisted throughout the treatment course.
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PMID:Treatment of psoriasis with chronic subcutaneous administration of somatostatin analog 201-995 (sandostatin). II. Effect on pancreatic and thyroid hormone. 240 89

In view of the emerging role of the phosphoinositide system in cellular communication we examined its involvement in quantal-transmitter release, which is a key element in synaptic transmission. Transmitter release is normally activated by an increase in intracellular calcium, achieved either by entry of calcium ions through the presynaptic membrane or by intracellular calcium liberation. One of the targets of the phosphoinositide signalling system is the enzyme protein kinase C (PKC), which can be activated experimentally by tumour promoting phorbol esters, including 12-O-tetradecanoylphorbol-13-acetate (TPA). Such activation of PKC may be implicated in transmitter release in two ways. First, phorbol esters were found to increase secretion and enhance calcium currents; it might therefore be expected that they would increase synaptic transmitter release. But phorbol esters also inhibit the calcium current in dorsal root ganglion neurones. We report that the phorbol ester TPA augments synaptic transmission at the neuromuscular junction by increasing transmitter liberation. Activation of PKC also depends synaptic depression.
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PMID:Activation of protein kinase C augments evoked transmitter release. 243 32

The failure to elicit cortical spreading depression (SD) under ketamine anesthesia has been examined in 25 rats. SD was elicited by microinjection of K+ acetate (1 microliter, 0.15 mol/l) into the cerebral cortex and monitored by recording the accompanying slow-potential waves. I.p. injection of ketamine HCl (50 mg/kg) elicited after 5-10 min blockade of SD propagation lasting 30-40 min. SD penetration into a cortical area superfused with 10(-4) and 10(-3) mol/l ketamine was partly or completely blocked, respectively. Systemic ketamine doses eliciting SD blockade only slightly reduced spontaneous activity of cortical units recorded with carbon fiber microelectrodes and did not increase but rather decreased the rate of K+ removal from a KCl pool (30 microliters, 40 mmol/l) contacting a 12.5 mm2 area of exposed cortical surface. The results indicate that the ketamine-induced SD blockade is due neither to epileptic activity nor to enhanced active transport of ions but rather to interference with chemically gated ionic channels and/or to stabilization of postsynaptic membranes.
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PMID:Ketamine blockade of cortical spreading depression in rats. 243 24

Ten healthy young males were studied with a double-blind, cross-over trial to determine whether or not chlormadinone acetate (CMA), a potent synthetic progesterone, augments hypoxic chemosensitivity. Seven days after CMA administration, inspiratory minute volume (VI) and tidal volume (VT) significantly increased. PaCO2 decreased by 3.0 +/- 2.6 (S.D.) Torr (p less than 0.05) and plasma bicarbonate decreased by 2.9 +/- 1.1 mM (p less than 0.01). During CMA administration, the atmospheric hypoxic ventilatory response (HVR), assessed by minute ventilatory (delta VI/delta SaO2), and occlusion pressure responses (delta P .2/delta SaO2), significantly increased about 1.9 (p less than 0.05) and 1.6 times (p less than 0.01) compared to the placebo response, respectively. The calculated normocapnic HVR (delta VI/delta SaO2) increased about 2.3 times the placebo run. Hypoxic response evaluated by the withdrawal test, which represents the peripheral chemosensitivity without involving the influence due to secondary hypoxic depression, was about 1.7 times the placebo response (p less than 0.05). We conclude that CMA augments hypoxic respiratory chemosensitivity.
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PMID:Effect of chlormadinone acetate, a synthetic progesterone, on hypoxic ventilatory response in men. 244 Oct 98

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