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. The effects of some divalent cations on the A-current (IA) in cultured rat dorsal root ganglion cells (DRGs) were studied using whole-cell patch recording. 2. IA was not affected by omission of calcium from the external medium; however it was significantly depressed by manganese (10 mM) applied by pressure ejection. This depressant effect of manganese resulted from a depolarizing shift of the activation curve by 17 mV, associated with only a slight reduction of the maximum conductance. At 10 mM manganese also caused a depolarizing shift of the steady-state inactivation curve by 34 mV. Divalent cations other than manganese also gave positive shifts of the steady-state activation and inactivation curves for IA but were of different potency; the sequence was: Cd2+ greater than Mn2+ = Co2+ greater than Mg2+. 3. A dose-response curve for the depolarizing shift of the activation and inactivation curves of IA, as a function of manganese concentration, could be fitted by a single binding site model with an apparent dissociation constant of approximately 17 mM. The depolarizing shift of the inactivation curve was on average twice as large as that of the activation curve. 4. In contrast to its effect on IA, manganese (10 mM) did not cause any appreciable change in the voltage dependence of the activation curve for the delayed rectifier K+ current. 5. A low concentration of manganese (1 mM) increased the amplitude of IA recorded at pre-pulse potentials ranging from -50 to -70 mV. This augmentation of IA resulted from a positive shift of the inactivation curve by 6 mV without an appreciable shift of the activation curve; as a result a population of A-channels is released from inactivation over pre-pulse potentials from -50 to -70 mV. 6. These results show that divalent cations can evoke a depolarizing shift of both the activation and inactivation gates controlling IA; this causes either depression or augmentation of IA, depending on the species and concentration of the divalent cation, and also on the pre- pulse potential used to de-inactivate IA. This modulatory effect of divalent cations on the gating of IA appears to reflect binding to a specific, saturable site, either the A-channel protein itself, or phospholipids electrically close to the gating apparatus.
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PMID:A modulatory action of divalent cations on transient outward current in cultured rat sensory neurones. 245 91

Monoclonal antibodies against gizzard smooth muscle myosin were generated and characterized. One of these antibodies, designated MM-2, recognized the 17-kDa light chain and modulated the ATPase activities and hydrodynamic properties of smooth muscle myosin. Rotary shadowing electron microscopy showed that MM-2 binds 51 (+/- 25) A from the head-rod junction. The depression of Ca2+- and Mg2+-ATPase activities of myosin and Ca2+-ATPase activity of heavy meromyosin at low KCl concentration were abolished by MM-2. Viscosity measurement indicated that MM-2 inhibits the transition of 6 S myosin to 10 S myosin. While the rate of the production of subfragment-1 by papain proteolysis of 6 S myosin was inhibited by MM-2, the rate of proteolysis of the heavy chain of 10 S myosin was enhanced by MM-2 and reached the same rate as that of 6 S myosin plus MM-2. These results suggest that MM-2 inhibits the formation of 10 S myosin by binding to the 17-kDa light chain which is localized at the head-neck region of the myosin molecule. MM-2 increased the Vmax of actin-activated Mg2+-ATPase activities of both dephosphorylated myosin and dephosphorylated heavy meromyosin about 10- and 20-fold, respectively. MM-2 also activated the actin-activated Mg2+-ATPase activity of phosphorylated myosin at a low MgCl2 concentration and thus abolished the Mg2+-dependence of acto phosphorylated myosin ATPase activity. These results suggest that MM-2 inhibits the formation of 10 S myosin, and this results in the activation of actin-activated Mg2+-ATPase activity even in the absence of phosphorylation.
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PMID:Inhibition of conformational change in smooth muscle myosin by a monoclonal antibody against the 17-kDa light chain. 246 45

Sarcoplasmic reticulum (SR) Ca2+ uptake and Ca2+-Mg2+-ATPase activity were examined in muscle homogenates and the purified SR fraction of the superficial and deep fibers of the gastrocnemius and vastus muscles of the rat after treadmill runs of 20 or 45 min or to exhaustion (avg time to exhaustion 140 min). Vesicle intactness and cross-contamination of isolated SR were estimated using a calcium ionophore and mitochondrial and sarcolemmal marker enzymes, respectively. Present findings confirm previously reported fiber-type specific depression in the initial rate and maximum capacity of Ca2+ uptake and altered ATPase activity after exercise. Depression of the Ca2+-stimulated ATPase activity of the enzyme was evident after greater than or equal to 20 min of exercise in SR isolated from the deep fibers of these muscles. The lowered ATPase activity was followed by a depression in the initial rate of Ca2+ uptake in both muscle homogenates and isolated SR fractions after greater than or equal to 45 min of exercise. Maximum Ca2+ uptake capacity was lower in isolated SR only after exhaustive exercise. Ca2+ uptake and Ca2+-sensitive ATPase activity were not affected at any duration of exercise in SR isolated from superficial fibers of these muscles; however, the Mg2+-dependent ATPase activity was increased after 45 min and exhaustive exercise bouts. The alterations in SR function could not be attributed to disrupted vesicles or differential contamination in the SR from exercise groups and were reinforced by similar changes in Ca2+ uptake in crude muscle homogenates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of exercise of varying duration on sarcoplasmic reticulum function. 252 76

Although oxygen free radicals have been implicated as mediators of cellular injury in myocardial ischemia-reperfusion, the exact nature of defects produced by these radicals is not clear. Because sarcolemmal Ca2+-pump is involved in the efflux of Ca2+ from the cell, this study was undertaken to examine the effects of oxygen free radicals on sarcolemmal ATP-dependent Ca2+ accumulation and Ca2+-stimulated Mg2+-dependent adenosinetriphosphatase (ATPase) activities as well as lipid peroxidation of membrane phospholipids. Isolated rat heart sarcolemmal membranes were incubated with xanthine + xanthine oxidase [a superoxide anion radical (O2-)-generating system], H2O2, or H2O2 + Fe2+ [a hydroxyl radical (HO.)-generating system] and assayed for Ca2+-pump activities. O2- inhibited the Ca2+-pump activities in a time-dependent manner; a significant inhibition of Ca2+-stimulated ATPase activity was seen after 1 min of incubation. Superoxide dismutase showed a protective effect on depression in Ca2+-pump activities caused by O2-.H2O2 inhibited Ca2+-pump activities in a dose-dependent manner; this inhibition was protected by the addition of catalase. HO. depressed the Ca2+-pump activities to a greater extent in comparison with H2O2. Mannitol showed a protective effect on HO.-induced inhibition of Ca2+-pump activities. The promotion of lipid peroxidation by free radicals was evident from increased formation of malondialdehyde. These results indicate that the sarcolemmal membrane is altered on exposure to oxygen free radicals, and this may result in depressing the Ca2+-pump mechanism for Ca2+ efflux from the myocardial cell.
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PMID:Depression of heart sarcolemmal Ca2+-pump activity by oxygen free radicals. 253 32

1. Propagated Ca-spikes were recorded from isolated cervical sympathetic nerve trunks of the rat when bathed in a solution containing 5 mM Ca2+, 0.5 or 1 microM tetrodotoxin (to block Na currents) and 1 mM 4-aminopyridine (to reduce K currents). 2. Spikes persisted when external Ca2+ was replaced with Sr2+ or Ba2+, but were blocked by the addition of the following inorganic Ca-channel blockers (in descending order of potency): Cd2+ greater than La3+ greater than Ni2+ greater than Co2+ greater than Mn2+ greater than Mg2+. 3. Ca-spike amplitude was reduced by up to 90% by (-)-noradrenaline (IC50 1.5 microM). The following sympathomimetic amines imitated this effect (in descending order of potency): clonidine greater than or equal to (-)-adrenaline greater than or equal to [(-)-noradrenaline] greater than or equal to dopamine greater than (-)-phenylephrine greater than or equal to (+/-)-amidephrine. 4. Ca-spike inhibition by (-)-noradrenaline was antagonized by phentolamine (pA2 6.5). Yohimbine was about 10 times weaker than phentolamine; (+/-)-propranolol (1 microM) and prazosin (10 microM) had no clear effect. 5. (-)-Noradrenaline reduced the amplitude of the compound action potential recorded from the superior cervical sympathetic ganglion following supramaximal preganglionic trunk stimulation when recorded in normal Krebs solution and hyperpolarized the ganglion with respect to the post-ganglionic trunk. Depression of the transmitted ganglionic action potential was antagonized by phentolamine (5 microM) but not by yohimbine (1 microM); in contrast 1 microM yohimbine completely prevented the ganglionic hyperpolarization. (-)-Noradrenaline did not hyperpolarize the preganglionic cervical sympathetic nerve trunk under these recording conditions. 6. It is suggested that inhibition of transmitter release from sympathetic preganglionic fibres produced by noradrenaline results from a depression of the voltage-gated Ca current in the fibres and/or their terminals, and that this action is mediated by an alpha-adrenoceptor which does not fully conform to either alpha 1 or alpha 2 subtypes.
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PMID:Inhibition of Ca-spikes in rat preganglionic cervical sympathetic nerves by sympathomimetic amines. 253 83

Hemisected mouse spinal cords were maintained in vitro and the concentrations of calcium [CA2+] and of magnesium [Mg2+] in the bath were varied. In control solution containing 1.2 mM of both [Ca2+] and [Mg2+] stimulation of a dorsal root (DR) evoked in an adjacent DR an initial fiber volley representing 'input'; a postsynaptic compound spike recorded by volume conduction from dorsal gray matter, the dorsal horn response (DHR); and a slow dorsal root potential (DRP). In the ventral root of the stimulated segment a monosynaptic reflex (VRR1) was evoked. The fiber volley was enhanced by lowering [Ca2+] or [Mg2+] and depressed when either ion concentration was raised. The DRP, DHR and VRR1 were enhanced in low [Mg2+] and in moderately elevated [Ca2+]. At 1.8 mM [Ca2+] and above, the 'classical' dorsal root reflex (DRR) and a GABA-dependent delayed VR reflex (VRR2) appeared. Transmission of reflexes was maximal between 2.4 and 3.6 mM [Ca2+], while DRP was maximal at about 4.8 mM. In elevated [Mg2+] and in low [Ca2+] all synaptically transmitted responses (DRR, DRP and VRR) were depressed. The influence of both [Ca2+] and [Mg2+] was stronger on DRP, DRR and VRR2 than on DHR and VRR1. The effects of simultaneous changes of [Ca2+] and [Mg2+] partially cancelled each other. We conclude that low to moderately elevated [Ca2+] mainly influences the release of transmitter from presynaptic terminals; at very high [Ca2+] the depression of neuronal excitability dominates. The effects of Ca2+ and Mg2+ on GABAergic transmission are especially marked.
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PMID:Changes in extracellular calcium and magnesium and synaptic transmission in isolated mouse spinal cord. 254 79

Two novel beta-(benzo[b]furan) analogues of baclofen (4-amino-3-benzo[b]furan-2-ylbutanoic acid, 9G, and 4-amino-3-(5-methoxybenzo[b]furan-2-yl)butanoic acid, 9H) antagonised the baclofen-induced depression of twitch contractions in the guinea-pig isolated ileum (estimated apparent pA2 3.9 and 4.1 respectively); both 9G and 9H also antagonised in a dose-dependent manner the baclofen-induced reduction of repetitive paroxysmal discharges in rat neo-cortical slice preparations maintained in Mg2+-free Krebs solution. These benzofurans evidently represents a new class of GABAB-receptor antagonist.
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PMID:Benzofuran analogues of baclofen: a new class of central and peripheral GABAB-receptor antagonists. 254 38

Superfusion of the isolated spinal cord of neonatal rats (4-9 days postpartum) with physiological medium containing 2-chloroadenosine (2-CA) or anoxic medium (equilibrated with 95% N2-5% CO2) depressed the evoked monosynaptic reflex (MSR) recorded extracellularly from a ventral spinal root. The effectiveness of 2-CA or anoxic medium in depressing the MSR was significantly reduced when the concentration of Mg2+ in the physiological medium was lowered from 1.25 X 10(-3) M to zero. The absence of Mg2+ resulted in a 7-fold shift to the right of the concentration-response curve to 2-CA and a reduction in the maximal depression of the MSR from 100% to 65 +/- 4% (mean +/- S.E.M.) of control. A 10 min exposure to anoxic medium containing 1.25 X 10(-3) M Mg2+ decreased the amplitude of the MSR to 23 +/- 6% of control, whilst in zero Mg2+ a decrease to only 50 +/- 5% of control was observed. These data provide further evidence that the response to adenosine, at the A1-receptor, is sensitive to Mg2+ ion concentration and suggest that there is an absolute requirement for Mg2+ in order to obtain full expression of the adenosine effect. Furthermore, the data are consistent with the hypothesis that adenosine is an important mediator of hypoxia-induced depression of the evoked MSR in the spinal cord, and suggest a potential role for Mg2+ during or after exposure to hypoxia in altering the actions of adenosine on neuronal activity or synaptic events.
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PMID:Effect of magnesium on depression of the monosynaptic reflex induced by 2-chloroadenosine or hypoxia in the isolated spinal cord of neonatal rats. 254 60

The effect of high dietary sulfur (S) supplementation on blood thiamine (B1) concentration, biochemical indices of liver, muscle and kidney damage and selected plasma electrolytes was studied in six sheep. Three of these sheep received an additional 230 mg thiamine/kg diet (Group 2). After approximately 2.5-3 weeks on this diet, all three sheep in the non-B1-supplemented group (Group 1) showed loss of appetite and developed mild neurological signs: depression, intermittent signs of excitation and head pressing. Increases in blood B1 concentration and plasma creatine kinase (CK) and aspartate aminotransferase (AST) were observed during this time in all affected animals. Clinical signs lasted only for two to five days. Sheep in group 2 were clinically normal throughout the experiment, but all of these animals also had elevated blood B1 concentrations and plasma CK activity at the 3 wk sampling. Plasma magnesium concentrations of group 1 sheep were elevated at the 2.5-3 wk and 6 wk samplings but they declined significantly (p less than 0.05) to low normal levels thereafter. Magnesium concentrations of group 2 sheep were low at the beginning but progressively increased during the course of the experiment. At necropsy, brain lesions suggestive of polioencephalomalacia (PEM) were observed in all sheep but were most marked in group 1. It is speculated that PEM may be caused by a direct toxic effect of S, S metabolites or B1 antimetabolites in the brain rather than by an in vivo B1 deficiency per se.
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PMID:Sulfur-induced polioencephalomalacia in sheep: some biochemical changes. 257 73

Magnesium and calcium concentrations were measured in the cerebrospinal fluid (CSF) of 15 neurological controls and 41 psychiatric patients suffering from major depression (n = 16), schizophrenic disorder (n = 15), or adjustment disorder (n = 10). All subjects were women 19-67 years of age and free from drugs at the time of the study. CSF was evaluated for 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), and cortisol (CS) levels, and all patients received a dexamethasone suppression test (DST) following lumbar puncture. CSF calcium levels did not differ among groups, although we found a trend toward higher mean levels in both depression and schizophrenia. By contrast, CSF magnesium was found to be significantly lower in both depression and adjustment disorder; if, however, patients who had made suicide attempts were excluded, the difference became insignificant. Patients who had made suicide attempts (by using either violent or nonviolent means) had significantly lower mean CSF magnesium level irrespective of the diagnosis. CSF calcium did not correlate with magnesium, 5-HIAA, HVA, CS, global severity, therapeutic response, or DST, but CSF magnesium correlated significantly with CSF 5-HIAA, especially after correcting for age and body height. Both variables seemed to be primarily related to recorded suicide attempts, but decreased magnesium was not limited to violent cases.
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PMID:Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts. 257 29

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