共查询到20条相似文献,搜索用时 31 毫秒
1.
A. Goldsworthy 《Journal of theoretical biology》1983,103(4):645-648
Because certain primitive behavioral responses in the large sea snail Aplysia have recently been linked to neurophysiological events at a synaptic level, special interest attaches to the role played by calcium ions at such synapses. Using an extended version of the model applied earlier to trace the flow of energy and information through a ganglion of the medicinal leech (Triffet &; Green, 1980), the authors investigate the electropotential effects of small transient localized changes in the calcium concentration near the inner membrane surface of a neuron in the resting state.When this state is well below the firing threshold, changes in Ca2+ concentration less than 10?8 M are shown to result only in low-level harmonic background oscillations. When the potential of the neurons is closer to threshold, however, and/or the Ca2+ concentration is of the order of 10?8 M, easily recognizable graded potentials appear, and these grow into firing peaks when the calcium concentration is increased still further.Though no attempt is made to deal with the amplification effects dependent on calcium-vesicle interactions and the related release of transmitter molecules, a unified mechanism for the underlying calcium ion dynamics is proposed. Graded potentials of increasing size are associated with a progressive localized thickening of the inner and outer Debye layers. Moreover, the transverse and longitudinal calcium currents set up in such regions prove adequate to account for both the depletion of Ca2+ ions necessary to achieve habituation, and the increase in their concentration required for sensitization. 相似文献
2.
Philip S Low 《生物化学与生物物理学报:生物膜》1978,514(2)
The specific modulation by three cations, Ca2+, Mg2+, and tetracaine of the equilibrium exchange of SO42− across the erythrocyte membrane was investigated. While external calcium had no effect on SO42− exchange, internal calcium, and external calcium in the presence of 10 μM A23187 were found to be potent inhibitors of the exchange reaction. The apparent inhibition constants (K1) for Ca2+ were calculated to be 6.1 μM and 5 μM for the above two conditions, respectively.Unlike Ca2+, Mg2+ was shown to be a weak activator of SO42− exchange with an apparent dissociation constant of 3.6 μM. Competition experiments demonstrated that the Ca2+ and Mg2+ sites associated with anion transport are distinct and noninteracting.Tetracaine, a cation at neutral pH, was also found to be an inhibitor of SO42− exchange with an apparent K1 of 0.8 mM. Although tetracaine was observed to displace calcium from non-specific sites on the erythrocyte membrane, it showed no effect on the apparent inhibition constant of Ca2+ for SO42− exchange. Thus, the Ca2+ and tetracaine sites also appear to be independent. The difficulty of situating three mutually independent sites on a single subunit protein, i.e., band 3, is considered.Using the experimental data obtained from five individuals, the concentration of free calcium in the red cell cytoplasm was calculated to range from 0.2 to 0.7 μM. This concentration was sufficient to reduce SO42− exchange only 3–8%. It was concluded that calcium inhibition of anion exchange, and, hence, impairment of CO2 transport, may be physiologically significant only in senescent cells and in certain types of anemia where calcium concentrations are significantly increased. 相似文献
3.
T-type Ca2+ channel family includes three subunits CaV3.1, CaV3.2 and CaV3.3 and have been shown to control burst firing and intracellular Ca2+ concentration ([Ca2+]i) in neurons. Here, we investigated whether CaV3.1 channels could generate a pacemaker current and contribute to cell excitability. CaV3.1 clones were over-expressed in the neuronal cell line NG108-15. CaV3.1 channel expression induced repetitive action potentials, generating spontaneous membrane potential oscillations (MPOs) and concomitant [Ca2+]i oscillations. These oscillations were inhibited by T-type channels antagonists and were present only if the membrane potential was around −61 mV. [Ca2+]i oscillations were critically dependent on Ca2+ influx through CaV3.1 channels and did not involve Ca2+ release from the endoplasmic reticulum. The waveform and frequency of the MPOs are constrained by electrophysiological properties of the CaV3.1 channels. The trigger of the oscillations was the CaV3.1 window current. This current induced continuous [Ca2+]i increase at −60 mV that depolarized the cells and triggered MPOs. Shifting the CaV3.1 window current potential range by increasing the external Ca2+ concentration resulted in a corresponding shift of the MPOs threshold. The hyperpolarization-activated cation current (Ih) was not required to induce MPOs, but when expressed together with CaV3.1 channels, it broadened the membrane potential range over which MPOs were observed. Overall, the data demonstrate that the CaV3.1 window current is critical in triggering intrinsic electrical and [Ca2+]i oscillations. 相似文献
4.
P. E. Lindahl 《Experimental cell research》1973,81(2):413-431
Mg2+, Ca2+ and Mn2+ were found to act as activators of the ATP-dependent surface reaction, leading to head-to-head association in bull spermatozoa. Ca2+ was more efficient than Mg2+, while Zn2+, like Na+ + K+ in combination with Mg2+, seemed to have no such effect. High ionic strength induced head-to-head association, as did higher concentrations of Mg2+ and Ca2+ than those necessary for the activation of ATP, Ca2+ acting in a lower conc. than Mg2+. To this effect was added that of the ATP-dependent reaction when ATP was also present. As activators, Mg2+ and Ca2+ did not potentiate each other; their effects were cumulative when the ions acted together.When the ATP concentration within the range 1 × 10−5 to 8 × 10−5 M was increased stepwise in the presence of 2 × 10−5 M Mg2+ or Ca2+, the association resulting from each single concentration step progressively increased. At low cation concentrations, the increase was about the same for the two cations: at higher concentrations it was much steeper in the presence of Ca2+ than in that of Mg2+. In the latter case, it was not statistically significant above 4 × 10−5 M ATP.Increasing the cation concentration in the range 1 × 10−5 to 4 × 10−5 M in the presence of 2 × 10−5 M ATP produced an immediate high increase in association, which was followed by a lower increase. The optimum concentration ratio for Mg2+:ATP was at least 1:1 and for Ca2+: ATP at least 1.5:1.Oubain, containing enone structure, abolishes association. 相似文献
5.
We have previously reported that angiotensin II (ANG II) induces oscillations in the cytoplasmic calcium concentration ([Ca2+]i) of pulmonary vascular myocytes. The present work was undertaken to investigate the effect of ANG II in comparison with ATP and caffeine on membrane currents and to explore the relation between these membrane currents and [Ca2+]i. In cells clamped at −60 mV, ANG II (10 μM) or ATP (100 μM) induced an oscillatory inward current. Caffeine (5 μM) induced only one transient inward current. In control conditions, the reversal potential (Erev) of these currents was close to the equilibrium potential for Cl− ions (ECl = −2.1 mV) and was shifted towards more positive values in low-Cl− solutions. Niflumic acid (10–50 μM) and DIDS (0.25-1 mM) inhibited this inward current. Combined recordings of membrane current and [Ca2+]i by Indo-1 microspectrofluorimetry revealed that ANG II- and ATP-induced currents occurred simultaneously with oscillations in [Ca2+]i, whereas the caffeine-induced current was accompanied by only one transient increase in [Ca2+]i Niflumic acid (25 μM) had no effect on agonist-induced [Ca2+]i responses, whereas thapsigargin (1 μM) abolished both membrane current and the [Ca2+]i response. Heparin (5 mg/ml in the pipette solution) inhibited both [Ca2+]i responses and membrane currents induced by ANG II and ATP, but not by caffeine. In pulmonary arterial strips, ANG II-induced contraction was inhibited by niflumic acid (25 μM) or nifedipine (1 μM) to the same extent and the two substances did not have an additive effect. This study demonstrates that, in pulmonary vascular smooth muscle, ANG II, as well as ATP, activate an oscillatory calcium dependent chloride current which is triggered by cyclic increases in [Ca2+]i and that both oscillatory phenomena are primarily IP3 mediated. It is suggested that ANG II-induced oscillatory chloride current could depolarise the cell membrane leading to activation of voltage-operated Ca2+ channels. The resulting Ca2+ influx contributes to the component of ANG II-induced contraction that is equally sensitive to chloride or calcium channel blockade. 相似文献
6.
Yixian Zhang Hong Xiao 《Mutation Research - Genetic Toxicology and Environmental Mutagenesis》1998,420(1-3)
The antagonistic effect of calcium (Ca2+), zinc (Zn2+) and selenium (Se4+) at different concentrations (10−2–10−6 M) against cadmium (Cd2+) induced genotoxic effects in root cells of Hordeum vulgare were studied. The results showed that 10−3–10−5 M could induce chromosomal aberrations and micronuclei formation. But in the treatment with 10−2–10−6 M of Ca2+, Zn2+ and Se4+ together with Cd2+ (10−3–10−5 M), respectively, the frequencies of chromosomal aberrations and micronuclei effectively decreased after 48 h of treatment. The treatment with 10−4–10−6 M of Ca2+ together with 10−4–10−5 M Cd2+, 10−6 M of Zn2+ together with 10−5 M Cd2+ and 10−6 M of Se4+ together with 10−5 M Cd2+ suggested rather obvious antagonistic effects. The order of the antagonisms of Ca2+, Se4+ and Zn2+ against Cd2+ toxicity was Ca2+>Se4+>Zn2+. The degree of antagonisms of Ca2+, Se4+ and Zn2+ against Cd2+ related to their concentration ratio. 相似文献
7.
J. Nagel-Volkmann C. Plieth D. Becker H. Lüthen K. Drffling 《Journal of plant physiology》2009,166(17):1955-1960
Relatively little is known about changes in the cytosolic free calcium ion concentration ([Ca2+]c) in monocotyledonous plants. Therefore, we produced transgenic winter wheat lines stably expressing the calcium-sensitive photoprotein aequorin constitutively in the cytosol. [Ca2+]c was detected in vivo by luminometry, and [Ca2+]c elevations were imaged at video rate. Experiments with the transgenic seedlings focused on potential changes in [Ca2+]c during cold exposure. Temperature-induced changes in [Ca2+]c were found to be more dependent on the change in temperature (dT dt−1) than on the absolute value of temperature. [Ca2+]c increased only at cooling rates higher than 8°C min−1, indicating that an overall cellular [Ca2+]c increase is of minor relevance as a signal for cold acclimation in wheat under ecological conditions. The results are discussed with regard to the so-called ‘calcium signature hypothesis’. 相似文献
8.
Nathaniel T. Blair J. Stefan Kaczmarek David E. Clapham 《The Journal of general physiology》2009,133(5):525-546
TRPC5 is a calcium (Ca2+)-permeable nonselective cation channel expressed in several brain regions, including the hippocampus, cerebellum, and amygdala. Although TRPC5 is activated by receptors coupled to phospholipase C, the precise signaling pathway and modulatory signals remain poorly defined. We find that during continuous agonist activation, heterologously expressed TRPC5 currents are potentiated in a voltage-dependent manner (∼5-fold at positive potentials and ∼25-fold at negative potentials). The reversal potential, doubly rectifying current–voltage relation, and permeability to large cations such as N-methyl-d-glucamine remain unchanged during this potentiation. The TRPC5 current potentiation depends on extracellular Ca2+: replacement by Ba2+ or Mg2+ abolishes it, whereas the addition of 10 mM Ca2+ accelerates it. The site of action for Ca2+ is intracellular, as simultaneous fura-2 imaging and patch clamp recordings indicate that potentiation is triggered at ∼1 µM [Ca2+]. This potentiation is prevented when intracellular Ca2+ is tightly buffered, but it is promoted when recording with internal solutions containing elevated [Ca2+]. In cell-attached and excised inside-out single-channel recordings, increases in internal [Ca2+] led to an ∼10–20-fold increase in channel open probability, whereas single-channel conductance was unchanged. Ca2+-dependent potentiation should result in TRPC5 channel activation preferentially during periods of repetitive firing or coincident neurotransmitter receptor activation. 相似文献
9.
Karl Kunzelmann Patthara Kongsuphol Fadi Aldehni Yuemin Tian Jiraporn Ousingsawat Richard Warth Rainer Schreiber 《Cell calcium》2009,46(4):233-241
In the past, a number of candidates have been proposed to form Ca2+ activated Cl− currents, but it is only recently that two families of proteins, the bestrophins and the TMEM16-proteins, recapitulate reliably the properties of Ca2+ activated Cl− currents. Bestrophin 1 is strongly expressed in the retinal pigment epithelium, but also at lower levels in other cell types. Bestrophin 1 may form Ca2+ activated chloride channels and, at the same time, affect intracellular Ca2+ signaling. In epithelial cells, bestrophin 1 probably controls receptor mediated Ca2+ signaling. It may do so by facilitating Ca2+ release from the endoplasmic reticulum, thereby indirectly activating membrane localized Ca2+-dependent Cl− channels. In contrast to bestrophin 1, the Ca2+ activated Cl− channel TMEM16A (anoctamin 1, ANO1) shows most of the biophysical and pharmacological properties that have been attributed to Ca2+-dependent Cl− channels in various tissues. TMEM16A is broadly expressed in both mouse and human tissues and is of particular importance in epithelial cells. Thus exocrine gland secretion as well as electrolyte transport by both respiratory and intestinal epithelia requires TMEM16A. Because of its role for Ca2+-dependent Cl− secretion in human airways, it is likely to become a prime target for the therapy of cystic fibrosis lung disease, caused by defective cAMP-dependent Cl− secretion. It will be very exciting to learn, how TMEM16A and other TMEM16-proteins are activated upon increase in intracellular Ca2+, and whether the other nine members of the TMEM16 family also form Cl− channels with properties similar to TMEM16A. 相似文献
10.
Hilda E. Witters Sylvain Van Puymbroeck Oscar L. J. Vanderborght 《Environmental Biology of Fishes》1992,34(2):197-206
Synopsis Adult rainbow trout, Oncorhynchus mykiss, were acutely exposed for 4 hours to low pH (4.4) and elevated Al-concentrations (300 µgI–1) in soft water (Ca2+ + Mg2+ = 25 µmolI–1). Comparison of branchial and renal ion fluxes (Na+, Cl–, Mg2+, Ca2+ and NH4
+) gave evidence that pH and Al effects were primarily localized at the gill site. The negative whole body ion balance seemed to be caused by stimulatory effects on Na and Cl efflux especially under Al stress and to a lesser extent by inhibition of influx. Measurements of gill potentials indicated positive shifts, which were similar in response to increasing levels of H+ ions and Al. It is suggested that Al-induced changes of branchial potentials causes high diffusable loss of ions through interference with membrane-bound Ca2+ at the gill site. 相似文献
11.
B. Vestergaard-Bogind 《生物化学与生物物理学报:生物膜》1983,730(2)
Ionophore A23187-mediated Ca2+-induced oscillations in the conductance of the Ca2+-sensitive K+ channels of human red cells were monitored with ion specific electrodes. The membrane potential was continuously reflected in CCCP-mediated pH changes in the buffer-free medium, changes in extracellular K+ activity were followed with a K+-selective electrode, and changes in the intracellular concentration of ionized calcium were calculated on the basis of cellular 45Ca content. An increased cellular 45Ca content at the successive minima of the oscillations where the K+ channels are closed indicates that the activation of the channels might be a (dCa2+/dt)-sensitive process and that accommodation to enhanced levels of intracellular free calcium may occur. An incipient inactivation of the K+ channels at intracellular ionized calcium levels of about 10 μM and a concurrent membrane potential of about −65 mV was observed. At a membrane potential of about −70 mV and an intracellular concentration of about 2·10−4M no inactivation of K+ channels took place. Inactivation of the K+ channels is suggested to be a compound function of the intracellular level of free calcium and the membrane potential. The observed sharp peak values in cellular 45Ca content support the notion that a necessary component of the oscillatory system is a Ca2+ pump operating with a significant delay in the activation/inactivation process in response to changes in cellular concentration of ionized calcium. 相似文献
12.
Peter J. Allen Molly A.H. Webb Eli Cureton Ronald M. Bruch Cameron C. Barth Stephan J. Peake W. Gary Anderson 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2009,154(4):437-450
Lake sturgeon, Acipenser fulvescens, are one of a few species of cartilaginous fishes that complete their life cycle entirely in freshwater. Sturgeons maintain very low concentrations of circulating calcium (Ca2+) compared with other vertebrates, and therefore, face unique challenges in regard to Ca2+ regulation, which are likely to be magnified during vitellogenic stages of the reproductive cycle. In the present study, Ca2+ concentrations and associated hormones of female and male lake sturgeon were examined in two wild populations, and were related to reproductive stage. In both populations, free, bound and total Ca2+ were low, peaking in mid-late vitellogenic females. Internal Ca2+ and phosphate (PO43−) concentrations were inversely related to environmental concentrations, suggesting that these ions are preferentially retained and that mechanisms for mobilization are up-regulated under diminished environmental concentrations. Plasma 17β-estradiol, 11-ketotestosterone and testosterone, peaked in mid-late vitellogenic females, while the androgens peaked in spawning males. Urine Ca2+ was more tightly regulated than other divalent ions and decreased in spawning fish. Therefore, the increases in free plasma Ca2+, the very low circulating concentrations of free and total Ca2+, and the increase in PO43− and bound Ca2+ in low Ca2+ environments indicate unique adaptations to Ca2+ regulation in the lake sturgeon. 相似文献
13.
Wallace Snipes James Cupp Jeffrey A Sands Alec Keith Alan Davis 《生物化学与生物物理学报:生物膜》1974,339(3):311-322
The bacteriophage PM2 requires extracellular Ca2+ at concentrations greater than 3 · 10−4 M for the production of viable virus, whereas the host cell Pseudomonas BAL-31 grows normally in medium containing 3 · 10−5 M Ca2+ (low calcium). Virus attachment occurs normally in low calcium, the infected cultures partially lyse, but no infectious virus particles are released. Sucrose gradient analysis shows that lysates made in low calcium contain no PM2-like particles. The addition of calcium very late in the infectious cycle completely restores virus production to cultures infected in low calcium, whereas removal of calcium after infection prevents virus production. Our experiments indicate that Ca2+ is essential for some process late in the lytic cycle, such as the final assembly of stable, infectious PM2 particles. 相似文献
14.
We studied on apple snail neurons the connection between K+ and Na+ concentration gradients, transmembrane difference of potentials, and concentrations of Ca2+ in the external medium. Sensitivity of the resting potential (RP) of neurons to the influence of temperature and to metabolic poisons rose considerably with a decrease of Ca2+ concentration in the solution surrounding a ganglion. An excess of Ca2+ in the external medium did not affect the RP or ion concentration in nerve cells. Removal of Na2+ from this solution causes hyperpolarization of the membrane which disappears when active transport of sodium ions through the membrane is suppressed. Sodium enrichment and potassium impoverishment of the neurons are observed in potassium-free solutions at 4°C. Reaccumulation of K+ and exclusion of Na+ from the solutions of 21°C depends on the concentration of Ca2+ in the medium. The ionic composition of the neurons is not restored upon removal of Ca2+ from the solution. Upon increasing the amount of Ca2+, movement of ions against the concentration gradients is intensified. Thus, it may be concluded that Ca2+ ions on the one hand participate in the maintenance of normal passive permeability of ions through the membrane, and on the other accelerate active transport of K+ and Na+ against the concentration gradients. The mechanisms of these processes are discussed.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 1, No. 3, pp. 323–330, November–December, 1969. 相似文献
15.
Abdelilah Arredouani Margarida Ruas Stephan C. Collins Raman Parkesh Frederick Clough Toby Pillinger George Coltart Katja Rietdorf Andrew Royle Paul Johnson Matthias Braun Quan Zhang William Sones Kenju Shimomura Anthony J. Morgan Alexander M. Lewis Kai-Ting Chuang Ruth Tunn Joaquin Gadea Lydia Teboul Paula M. Heister Patricia W. Tynan Elisa A. Bellomo Guy A. Rutter Patrik Rorsman Grant C. Churchill John Parrington Antony Galione 《The Journal of biological chemistry》2015,290(35):21376-21392
Pancreatic β cells are electrically excitable and respond to elevated glucose concentrations with bursts of Ca2+ action potentials due to the activation of voltage-dependent Ca2+ channels (VDCCs), which leads to the exocytosis of insulin granules. We have examined the possible role of nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated Ca2+ release from intracellular stores during stimulus-secretion coupling in primary mouse pancreatic β cells. NAADP-regulated Ca2+ release channels, likely two-pore channels (TPCs), have recently been shown to be a major mechanism for mobilizing Ca2+ from the endolysosomal system, resulting in localized Ca2+ signals. We show here that NAADP-mediated Ca2+ release from endolysosomal Ca2+ stores activates inward membrane currents and depolarizes the β cell to the threshold for VDCC activation and thereby contributes to glucose-evoked depolarization of the membrane potential during stimulus-response coupling. Selective pharmacological inhibition of NAADP-evoked Ca2+ release or genetic ablation of endolysosomal TPC1 or TPC2 channels attenuates glucose- and sulfonylurea-induced membrane currents, depolarization, cytoplasmic Ca2+ signals, and insulin secretion. Our findings implicate NAADP-evoked Ca2+ release from acidic Ca2+ storage organelles in stimulus-secretion coupling in β cells. 相似文献
16.
Dezs? Boda Mónika Valiskó Douglas Henderson Bob Eisenberg Dirk Gillespie Wolfgang Nonner 《The Journal of general physiology》2009,133(5):497-509
A physical model of selective “ion binding” in the L-type calcium channel is constructed, and consequences of the model are compared with experimental data. This reduced model treats only ions and the carboxylate oxygens of the EEEE locus explicitly and restricts interactions to hard-core repulsion and ion–ion and ion–dielectric electrostatic forces. The structural atoms provide a flexible environment for passing cations, thus resulting in a self-organized induced-fit model of the selectivity filter. Experimental conditions involving binary mixtures of alkali and/or alkaline earth metal ions are computed using equilibrium Monte Carlo simulations in the grand canonical ensemble. The model pore rejects alkali metal ions in the presence of biological concentrations of Ca2+ and predicts the blockade of alkali metal ion currents by micromolar Ca2+. Conductance patterns observed in varied mixtures containing Na+ and Li+, or Ba2+ and Ca2+, are predicted. Ca2+ is substantially more potent in blocking Na+ current than Ba2+. In apparent contrast to experiments using buffered Ca2+ solutions, the predicted potency of Ca2+ in blocking alkali metal ion currents depends on the species and concentration of the alkali metal ion, as is expected if these ions compete with Ca2+ for the pore. These experiments depend on the problematic estimation of Ca2+ activity in solutions buffered for Ca2+ and pH in a varying background of bulk salt. Simulations of Ca2+ distribution with the model pore bathed in solutions containing a varied amount of Li+ reveal a “barrier and well” pattern. The entry/exit barrier for Ca2+ is strongly modulated by the Li+ concentration of the bath, suggesting a physical explanation for observed kinetic phenomena. Our simulations show that the selectivity of L-type calcium channels can arise from an interplay of electrostatic and hard-core repulsion forces among ions and a few crucial channel atoms. The reduced system selects for the cation that delivers the largest charge in the smallest ion volume. 相似文献
17.
Twin-electrode voltage-clamp techniques were used to study the effect of calcium and calcium channel blockers on the transient
outward current in isolated F76 and D1 neurones of Helix aspersa subesophageal ganglia in vitro (soma only preparation with no cell processes). On lowering extracellular Ca2+ concentration from 10 to 2 mm or removing extracellular calcium from the bathing medium, the threshold for this current shifted in a negative direction
by 11.5 and 20 mV, respectively. On the other hand, increasing the extracellular Ca2+ concentration from 10 to 20 and to 40 mm shifted the steady-state inactivation curves in positive directions on the voltage axis by 7 and 15 mV, respectively. Upon
application of calcium channel blockers, Co2+, La3+, Ni2+ and Cd2+, transient potassium current amplitude was reduced in a voltage-dependent manner, being more effective at voltages close
to the threshold. The current was elicited even at a holding potential of −34 mV. The specific calcium channel blockers, amiloride
and nifedipine did not shift the activation and steady-state inactivation curves and did not reduce the transient outward
current amplitude. It was concluded that the transient outward current is not dependent on intracellular Ca2+ but that it is modulated by Ca2+ and di- and trivalent ions extracellularly. The effects of these ions are very unlikely to be due to a surface charge effect
because the addition of La3+ (200 μm) completely reverses the shift in a hyperpolarizing direction when the extracellular Ca2+ concentration was reduced from 10 to 1 mm and additionally shifts the kinetics further still in a depolarizing direction. The responses seen here are consistent with
a specific effect of di- and trivalent ions on the transient outward current channels leading to a modification of gating.
Received: 30 March 1999/Revised: 5 October 1999 相似文献
18.
Fumio Hayashi Masahiro Sokabe Masayuki Takagi Kohei Hayashi Uichiro Kishimoto 《生物化学与生物物理学报:生物膜》1978,510(2):305-315
A calcium sensitive univalent cation channel could be formed by lysotriphosphoinositide on an artificial bilayer membrane made of oxidized cholesterol. The modified membrane was selectively permeable to univalent cations, but was only very sparingly permeable to anions or divalent cations. Selectivity sequence among group IA cations was Rb+ > Cs+ > Na+ > K+ > Li+. The conductance of the membrane was increased up to a value of about 10−2 ohm−1/cm2 with an increase in the concentration of univalent cation, and was drastically depressed by a relatively small increase in the concentration of calcium ion or other divalent cations. The sequence of depressing efficiency among divalent cations was Zn2+ > Cd2+ > Ca2+ > Sr2+ > Mg2+. 相似文献
19.
Structural roles of functional Ca2+ and Cl− ions in photosynthetic oxygen-evolving complexes (OEC) were studied using low- (640–350 cm−1) and mid- (1800–1200 cm−1) frequency S2/S1 Fourier transform infrared (FTIR) difference spectroscopy. Studies using highly active Photosystem (PS) II core particles from spinach enabled the detection of subtle spectral changes. Ca2+-depleted and Ca2+-reconstituted particles produced very similar mid- and low-frequency spectra. The mid-frequency spectrum was not affected by reconstitution with 44Ca isotope. In contrast, Sr2+-substituted particles showed unique spectral changes in the low-frequency Mn–O–Mn mode at 606 cm−1 as well as in the mid-frequency carboxylate stretching modes. The mid-frequency spectrum of Cl−-depleted OEC exhibited marked changes in the carboxylate stretching modes and the suppression of protein modes compared with that of Cl−-reconstituted OEC. However, Cl−-depletion did not exert significant effects on the low-frequency spectrum. 相似文献
20.
Natalia López-del Hoyo Santiago López-Begines Jose Luis Rosa Jeannie Chen Ana Méndez 《PLoS genetics》2014,10(7)
The neuronal calcium sensor proteins GCAPs (guanylate cyclase activating proteins) switch between Ca2+-free and Ca2+-bound conformational states and confer calcium sensitivity to guanylate cyclase at retinal photoreceptor cells. They play a fundamental role in light adaptation by coupling the rate of cGMP synthesis to the intracellular concentration of calcium. Mutations in GCAPs lead to blindness. The importance of functional EF-hands in GCAP1 for photoreceptor cell integrity has been well established. Mutations in GCAP1 that diminish its Ca2+ binding affinity lead to cell damage by causing unabated cGMP synthesis and accumulation of toxic levels of free cGMP and Ca2+. We here investigate the relevance of GCAP2 functional EF-hands for photoreceptor cell integrity. By characterizing transgenic mice expressing a mutant form of GCAP2 with all EF-hands inactivated (EF−GCAP2), we show that GCAP2 locked in its Ca2+-free conformation leads to a rapid retinal degeneration that is not due to unabated cGMP synthesis. We unveil that when locked in its Ca2+-free conformation in vivo, GCAP2 is phosphorylated at Ser201 and results in phospho-dependent binding to the chaperone 14-3-3 and retention at the inner segment and proximal cell compartments. Accumulation of phosphorylated EF−GCAP2 at the inner segment results in severe toxicity. We show that in wildtype mice under physiological conditions, 50% of GCAP2 is phosphorylated correlating with the 50% of the protein being retained at the inner segment. Raising mice under constant light exposure, however, drastically increases the retention of GCAP2 in its Ca2+-free form at the inner segment. This study identifies a new mechanism governing GCAP2 subcellular distribution in vivo, closely related to disease. It also identifies a pathway by which a sustained reduction in intracellular free Ca2+ could result in photoreceptor damage, relevant for light damage and for those genetic disorders resulting in “equivalent-light” scenarios. 相似文献