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Ca2+ Content (ca2+ + content)
Selected AbstractsPhysiological Responses of Krishum (Iris lactea Pall. var. chinensis Koidz) to Neutral and Alkaline SaltsJOURNAL OF AGRONOMY AND CROP SCIENCE, Issue 6 2008Y. Wang Abstract The aims of this study were to compare the physiological responses of krishum (Iris lactea Pall. var. chinensis Koidz) to neutral and alkaline salt stress and identify and examine the mechanisms involved in plant response to salt treatments. In this study, biomass, ion accumulation (Na+, K+, Ca2+, Mg2+), organic solute (proline) concentration, rate of membrane electrolyte leakage (REL) and antioxidase activities including those of superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6) and peroxidase (POD, EC 1.11.1.7) were investigated in krishum under different concentrations of NaCl, Na2CO3 and the mixture of the two salts in the same volume. All three treatments caused increases in Na+ concentration, proline content and REL and decreases in root Mg2+ and K+ content. Increased Ca2+ and antioxidase activities were observed at lower external Na+ concentrations. However, at higher external Na+ levels, decreased Ca2+ and antioxidase activities were detected. Alkaline salt resulted in more damage to krishum than neutral salt including lower SOD, POD and CAT activities and decreased proline content, relative to neutral salt. High Na+ and low K+ in krishum intensified ion toxicity under alkaline condition. Alkaline salt caused greater harm to plants than neutral salt, the primary reason of which might be the lower Ca2+ content in the plant under alkaline salt stress. [source] ,-Synuclein modulation of Ca2+ signaling in human neuroblastoma (SH-SY5Y) cellsJOURNAL OF NEUROCHEMISTRY, Issue 5 2009Nishani T. Hettiarachchi Abstract Parkinson's disease (PD) is characterized in part by the presence of ,-synuclein (,-syn) rich intracellular inclusions (Lewy bodies). Mutations and multiplication of the ,-synuclein gene (SNCA) are associated with familial PD. Since Ca2+ dyshomeostasis may play an important role in the pathogenesis of PD, we used fluorimetry in fura-2 loaded SH-SY5Y cells to monitor Ca2+ homeostasis in cells stably transfected with either wild-type ,-syn, the A53T mutant form, the S129D phosphomimetic mutant or with empty vector (which served as control). Voltage-gated Ca2+ influx evoked by exposure of cells to 50 mM K+ was enhanced in cells expressing all three forms of ,-syn, an effect which was due specifically to increased Ca2+ entry via L-type Ca2+ channels. Mobilization of Ca2+ by muscarine was not strikingly modified by any of the ,-syn forms, but they all reduced capacitative Ca2+ entry following store depletion caused either by muscarine or thapsigargin. Emptying of stores with cyclopiazonic acid caused similar rises of [Ca2+]i in all cells tested (with the exception of the S129D mutant), and mitochondrial Ca2+ content was unaffected by any form of ,-synuclein. However, only WT ,-syn transfected cells displayed significantly impaired viability. Our findings suggest that ,-syn regulates Ca2+ entry pathways and, consequently, that abnormal ,-syn levels may promote neuronal damage through dysregulation of Ca2+ homeostasis. [source] Glutamate-mediated influx of extracellular Ca2+ is coupled with reactive oxygen species generation in cultured hippocampal neurons but not in astrocytesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1-2 2005Stefan Kahlert Abstract Generation of reactive oxygen species (ROS) in brain tissue leads to neurodegeneration. The major source of ROS is the mitochondrial respiratory chain. We studied regulation of Ca2+ level, mitochondrial potential, and ROS generation in defined mixed hippocampal cell cultures exposed to glutamate (100 ,M). Recordings were made from individually identified astrocytes and neurons to compare the physiologic responses in both cell types. Neurons identified by synaptotagmin immunoreactivity were characterized functionally by the fast Ca2+ increase with K+ (50 mM) stimulation, and the astrocytes identified by glial fibrillary acidic protein (GFAP) staining had the functional characteristic of a transient Ca2+ peak in response to ATP (10 ,M) stimulation. We found that the glutamate-mediated Ca2+ response in neurons is due largely to influx of extracellular Ca2+. This is consistent with our finding that in cultured hippocampal neurons, stores depending on the activity of the sarcoendoplasmic reticulum Ca2+ ATPase (SERCA) pump had a low Ca2+ content, regardless of whether the neurons were challenged or not with K+ before applying the SERCA inhibitor cyclopiazonic acid (CPA). Astrocytes displayed a large CPA-mediated Ca2+ response, indicating a high level of Ca2+ load in the stores in astrocytes. Importantly, the rise in ROS generation due to glutamate application was cell-type specific. In neurons, glutamate induced a marked rise in generation of ROS, but not in astrocytes. In both astrocytes and neurons, the mitochondrial potential was increased in response to glutamate challenge. We conclude that in neurons, Ca2+ influx accounts for the increased ROS generation in response to glutamate. This might explain the high vulnerability of neurons to glutamate challenge compared to the vulnerability of astrocytes. The high resistance of astrocytes is accompanied by an efficient downregulation of cytosolic Ca2+, which is not found in neurons. © 2004 Wiley-Liss, Inc. [source] The controlled release behavior and pH- and thermo-sensitivity of alginate/poly(vinyl alcohol) blended hydrogelsPOLYMERS FOR ADVANCED TECHNOLOGIES, Issue 8 2009Win-Chun Jao Abstract Poly(vinyl alcohol) (PVA) was blended with sodium alginate (Alg) in various ratios and crosslinked with calcium chloride and made into hydrogel membranes. The dependence of the swelling behavior of these Alg-Ca/PVA hydrogels on pH was investigated. The temperature-dependent swelling behavior of the semi-interpenetrating network (semi-IPN) hydrogels was examined at temperatures from 2 to 45°C and the enthalpy of mixing (,Hmix) was determined at various temperatures. The molecular structure of the hydrogels was studied by infrared spectroscopy and their water structure in the semi-IPN hydrogels was measured by differential scanning calorimetry (DSC). The influence of Ca2+ content on the network structure of Alg-Ca/PVA hydrogels was investigated in terms of the compressive elastic modulus, effective crosslinking density, and the polymer,solvent interaction parameter based on the Flory theory. The loading of alizarin red S (ARS) followed the Langmuir isotherm mechanism and the release kinetics of ARS from the Alg-Ca/PVA hydrogels followed the Fickian diffusion mechanism. Copyright © 2008 John Wiley & Sons, Ltd. [source] Evolution and modulation of intracellular calcium release during long-lasting, depleting depolarization in mouse muscleTHE JOURNAL OF PHYSIOLOGY, Issue 19 2008Leandro Royer Intracellular calcium signals regulate multiple cellular functions. They depend on release of Ca2+ from cellular stores into the cytosol, a process that in many types of cells appears to be tightly controlled by changes in [Ca2+] within the store. In contrast with cardiac muscle, where depletion of Ca2+ in the sarcoplasmic reticulum is a crucial determinant of termination of Ca2+ release, in skeletal muscle there is no agreement regarding the sign, or even the existence of an effect of SR Ca2+ level on Ca2+ release. To address this issue we measured Ca2+ transients in mouse flexor digitorum brevis (FDB) skeletal muscle fibres under voltage clamp, using confocal microscopy and the Ca2+ monitor rhod-2. The evolution of Ca2+ release flux was quantified during long-lasting depolarizations that reduced severely the Ca2+ content of the SR. As in all previous determinations in mammals and non-mammals, release flux consisted of an early peak, relaxing to a lower level from which it continued to decay more slowly. Decay of flux in this second stage, which has been attributed largely to depletion of SR Ca2+, was studied in detail. A simple depletion mechanism without change in release permeability predicts an exponential decay with time. In contrast, flux decreased non-exponentially, to a finite, measurable level that could be maintained for the longest pulses applied (1.8 s). An algorithm on the flux record allowed us to define a quantitative index, the normalized flux rate of change (NFRC), which was shown to be proportional to the ratio of release permeability P and inversely proportional to Ca2+ buffering power B of the SR, thus quantifying the ,evacuability' or ability of the SR to empty its content. When P and B were constant, flux then decayed exponentially, and NFRC was equal to the exponential rate constant. Instead, in most cases NFRC increased during the pulse, from a minimum reached immediately after the early peak in flux, to a time between 200 and 250 ms, when the index was no longer defined. NFRC increased by 111% on average (in 27 images from 18 cells), reaching 300% in some cases. The increase may reflect an increase in P, a decrease in B, or both. On experimental and theoretical grounds, both changes are to be expected upon SR depletion. A variable evacuability helps maintain a constant Ca2+ output under conditions of diminishing store Ca2+ load. [source] Cardioprotection afforded by chronic exercise is mediated by the sarcolemmal, and not the mitochondrial, isoform of the KATP channel in the ratTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005David A. Brown This study was conducted to examine the role of myocardial ATP-sensitive potassium (KATP) channels in exercise-induced protection from ischaemia,reperfusion (I,R) injury. Female rats were either sedentary (Sed) or exercised for 12 weeks (Tr). Hearts were excised and underwent a 1,2 h regional I,R protocol. Prior to ischaemia, hearts were subjected to pharmacological blockade of the sarcolemmal KATP channel with HMR 1098 (SedHMR and TrHMR), mitochondrial blockade with 5-hydroxydecanoic acid (5HD; Sed5HD and Tr5HD), or perfused with buffer containing no drug (Sed and Tr). Infarct size was significantly smaller in hearts from Tr animals (35.4 ± 2.3 versus 44.7 ± 3.0% of the zone at risk for Tr and Sed, respectively). Mitochondrial KATP blockade did not abolish the training-induced infarct size reduction (30.0 ± 3.4 versus 38.0 ± 2.6 in Tr5HD and Sed5HD, respectively); however, sarcolemmal KATP blockade completely eradicated the training-induced cardioprotection. Infarct size was 71.2 ± 3.3 and 64.0 ± 2.4% of the zone at risk for TrHMR and Sed HMR. The role of sarcolemmal KATP channels in Tr-induced protection was also supported by significant increases in both subunits of the sarcolemmal KATP channel following training. LV developed pressure was better preserved in hearts from Tr animals, and was not influenced by addition of HMR 1098. 5HD decreased pressure development regardless of training status, from 15 min of ischaemia through the duration of the protocol. This mechanical dysfunction was likely to be due to a 5HD-induced increase in myocardial Ca2+ content following I,R. The major findings of the present study are: (1) unlike all other known forms of delayed cardioprotection, infarct sparing following chronic exercise was not abolished by 5HD; (2) pharmacological blockade of the sarcolemmal KATP channel nullified the cardioprotective benefits of exercise training; and (3) increased expression of sarcolemmal KATP channels was observed following chronic training. [source] Effects of chlorpromazine on excitation,contraction coupling events in fast-twitch skeletal muscle fibres of the ratBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2004R Wagner Single mechanically skinned fibres from the rat extensor digitorum longus muscle, which allow access to intracellular compartments, were used to examine the effects of 0.5,100 ,M chlorpromazine hydrochloride (CPZ) on the major steps of the excitation,contraction (E,C) coupling to elucidate the involvement of skeletal muscle in the neuroleptic malignant syndrome (NMS). At 1 ,M, CPZ caused a 20,30% increase in the force response induced by t-system depolarisation and a marked increase in the rate of caffeine-induced SR Ca2+ release. At [CPZ]2.5 ,M, there was an initial increase followed by a marked decrease of the t-system depolarisation-induced force responses, while the potentiating effect on the caffeine-induced SR Ca2+ release remained. These effects were reversible. CPZ had no effect on the maximum Ca2+ -activated force, but caused reversible, concentration-dependent increases in the Ca2+ sensitivity of the contractile apparatus at [CPZ] 10 ,M, with a 50% predicted shift of 0.11 pCa (,log [Ca2+]) units at 82.3 ,M CPZ. CPZ did not alter the rate of SR-Ca2+ loading at 1 and 10 ,M, but reversibly reduced it by ,40% at 100 ,M by reducing the SR Ca2+ pump. Nevertheless, the SR Ca2+ content was greater when fibres became unresponsive to t-system-induced depolarisation in the presence than in the absence of 100 ,M CPZ. The results show that CPZ has concentration-dependent stimulatory and inhibitory effects on various steps of the E,C coupling, which can explain the involvement of skeletal muscle in NMS and reconcile previous divergent data on CPZ effects on muscle. British Journal of Pharmacology (2004) 141, 624,633. doi:10.1038/sj.bjp.0705655 [source] Oscillatory transient inward currents in ventricular myocytes of healthy versus myopathic Syrian hamsterCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2004Sze-Hsueh Wu Summary 1.,The present experiments were performed in order to study abnormal action potential configuration and ion channel activity in ventricular myocytes obtained from 23 male myopathic Syrian hamsters (Biobreeders strain 14.6, 32,52 weeks old) compared with 10 age-matched healthy control hamsters (Biobreeders F1B) by means of whole-cell patch-clamp techniques. 2.,The results show that the myopathic myocytes had a longer action potential duration, a reduced transient outward K+ current on depolarization and a smaller transient inward current on repolarization after prolonged depolarizing pulses (> 500 msec). However, the L-type Ca2+ current and the inwardly rectifing K+ current were not significantly different from those of healthy myocytes. 3.,The oscillatory transient inward currents could be diminished by treatment with ryanodine (0.01,1 µmol/L), a sarcoplasmic reticulum (SR) Ca2+ release channel blocker, or with Na+ -free superfusate. 4.,We conclude that the hereditary myopathic hamsters are less likely to develop delayed afterdepolarization-related transient inward currents and triggered arrhythmias owing to a smaller SR Ca2+ content. [source] Tonic Potentiation And Attenuation Produced By Membrane Depolarization In Guinea-Pig TrachealisCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2000Kenichi Yamaki SUMMARY 1. We studied how membrane depolarization directly affected intracellular Ca2+ signalling when voltage-operated Ca2+ channels (VOCC) were not available in guinea-pig tracheal smooth muscle. To block VOCC, we used 3 ,mol/L verapamil, which completely abolished high K+ (20,60 mmol/L)-induced contraction, and elevation of fura-2 signal. 2. Muscle tone was generated by adding Ca2+ to the extracellular Ca2+ -free solution containing prostaglandin (PG)E2 (100 nmol/L) after abolishing basal tone with indomethacin (1 ,mol/L). 3. In the absence of verapamil, high K+ (20,60 mmol/L) solution potentiated 2.4 mmol/L Ca2+ -induced sustained contractions. Even in the presence of 3 ,mol/L verapamil, replacement with 20 and 40 mmol/L K+ solution induced tonic potentiation, which was changed to attenuation with a higher K+ solution (60 mmol/L), lower extracellular Ca2+ concentration ([Ca2+]o) and pretreatment with cyclopiazonic acid (10 ,mol/L), a Ca2+ sequestration inhibitor. 4. These results indicate that the balance between depolarization-dependent Ca2+ release and receptor-operated cation channel inhibition may determine whether tonic potentiation or attenuation is manifested, depending on the availability of VOCC, the magnitude of the depolarization, [Ca2+]o and Ca2+ content in the sarcoplasmic reticulum. [source] | |||||||||||||