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1.
Mariano Julián Rodriguez Carlos Bernardo Perez-Etchegoyen Lidia Szczupak 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2009,195(5):491-500
Recent work indicated that co-activity of different motoneurons (MNs) in the leech can be regulated through a network that
is centered on a pair of nonspiking (NS) neurons. Here, we investigate whether this effect generalizes to different types
of MNs that display differential co-activity patterns in different motor behaviors: the dorsal longitudinal excitors DE-3
and the dorsal and ventral excitors MN-L. The data indicates that both motoneurons are coupled to the NS neurons through rectifying
junctions that are activated when the motoneuron membrane potential becomes more negative than that of the NS, and that they
exert an inhibitory synaptic potential on NS via a polysynaptic pathway. In addition, DE-3 and MN-L are linked by junctions
that allow mutual excitation but the transmission of excitatory signals from MN-L to DE-3 depended on NS membrane potential.
The results support the view that NS neurons can play a central role in orchestrating the co-activity of MNs during motor
behaviors. 相似文献
2.
S. A. Menzikov N. N. Ruzhinskaya O. V. Menzikova 《Journal of Evolutionary Biochemistry and Physiology》2000,36(3):346-352
Effects of γ-aminobutyric acid (GABA) and ethanol on Mg2+-ATPase from mitochondrial and microsomal fractions of the fish brain were studied. GABA (10-8–10-4 M) activates microsomal Mg2+-ATPase, but has no effect on the mitochondrial enzyme activity. This effect of GABA on the microsomal Mg2+-ATPase was absent in the presence of 8% ethanol. Ethanol at 1– 10% concentrations inhibits the basal microsomal Mg2+-ATPase and has no effect on the mitochondria enzyme. Using cytochemical technique, Mg2+-ATPase was revealed both in neurons and in glial cells. The ethanol-sensitive Mg2+-ATPase is located in the area of synaptic junctions and is bound to plasma, vesicular, and smooth endoplasmic reticulum membranes. 相似文献
3.
G. Benzi A. Gorini B. Ghigini A. Moretti F. Dagani R. F. Villa 《Neurochemical research》1996,21(1):7-18
The changes in the Mg2+-dependent V-type ATPase activity and the Mg2+-ATP-dependent H+ pumping activity of the synaptic vesicles from the cerebral cortex of rats submitted to intermittent chronic (4 weeks) mild
or severe hypoxia were evaluated. The adaptation to the chronic severe hypoxia increases both the ATPase and the H+ pumping activities which are inhibited by NEM with an exponential relationship between the IC50 values and the in vivo O2 concentration. The Mg2+-dependent increase in H+ pumping activity of synaptic vesicles from the rats subjected to in vivo chronic hypoxia may be antagonized by nigericin
(dissipating ΔpH) and by FCCP (dissipating ΔpH and ΔΨSV). In contrast, valinomycin (dissipating the ΔΨSV and facilitating an enhancement in ΔpH) increases in vitro the H+ pumping activity that is inhibited by the addition of high concentration of K gluconate (reducing the rate of K+ efflux). The preincubation of vesicles from hypoxic rats with FCCP, but not with nigericin, inhibits the valinomycin-increased
H+ pumping activity.l-glutamate increases the H+ pumping activity in synaptic vesicles from the cerebral cortex of chronic hypoxic rats, whereas other amino acids (i.e.,l-aspartate andl-homocysteate) and glutamate analogs (i.e., quisqualate and ibotenate) are ineffective. The adaptation to both chronic intermittent
severe hypoxia and in vivo treatment with posatireline causes a decrease in the Mg2+-ATPase activity consistent with the decrease in the H+ pumping one of the synaptic vesicles. The addition of nigericin into incubation medium magnifies the decrease in the H+ pumping activity, while the addition of FCCP is ineffective, suggesting that the treatment with posatireline interferes with
the ΔΨSV component in the
of the synaptic vesicles from rats submitted to chronic hypoxia. The results of the in vivo and in vitro experiments suggest
that in the synaptic vesicles from hypoxic rats the ΔΨSV component in
may be most effective in increasing the Mg2+-ATP-dependent H+ pumping activity. 相似文献
4.
In this review, we discuss the function and modulation of chloride-selective glycine receptor (GlyR) channels, some genetic
diseases originated from dysfunction of GlyRs, and modulation of glycinergic synapses by intracellular calcium (Ca2+) with particular attention on the motoneurons of the hypoglossal nucleus. This motor nucleus is a brainstem structure implicated
in the command of coordinated movements during oral behavioral phenomena, including feeding, drinking, grooming, and respiration.
In this nucleus, more than 90% of its cells are motoneurons. These hypoglossal motoneurons (HMs) are involved in a variety
of motor functions and exhibit two remarkable features: (i) a low endogenous Ca2+ buffering capacity, which determines the rapid dynamics of cytosolic intracellular Ca2+, and (ii) powerful glycinergic inputs, which determine the main inhibitory drive on the above cells in adult animals. Glycine
receptors belong to the superfamily of Cys-loop ligand-gated ion channels. They are capable of forming functional homo-or
heteromeric chloride-selective channels. Dysfunction of GlyRs results in a genetic neurological motor disorders, including
hyperekplexia. These diseases originate from mutations in the GlyR gene, leading to a decrease in single channel conductance,
a lower affinity to the neurotransmitter, or a low level of GlyR expression. The function of glycinergic synapses is modulated
during developmental changes and strictly controlled by several feedback mechanisms at pre-and post-synaptic levels. The developmental
modulation consists in switch in the GlyR subunit composition and change in the chloride homeostasis during the synaptic maturation
and formation of inhibitory networks. Retrograde signalling plays an important role in the synaptic function of HMs; it provides
post-synaptic neurons with efficient tools for controlling pre-synaptic afferents. Glycine receptors and glycinergic synapses
are also regulated by intracellular Ca2+. The mechanisms of these modulations are discussed.
Neirofiziologiya/Neurophysiology, Vol. 39, Nos. 4/5, pp. 338–349, July–October, 2007. 相似文献
5.
Effects of intracellular Mg2+ on a native Ca2+-and voltage-sensitive large-conductance K+ channel in cultured human renal proximal tubule cells were examined with the patch-clamp technique in the inside-out mode.
At an intracellular concentration of Ca2+ ([Ca2+]i) of 10−5–10−4 M, addition of 1–10 mM Mg2+ increased the open probability (Po) of the channel, which shifted the Po –membrane potential (Vm) relationship to the negative voltage direction without causing an appreciable change in the gating charge (Boltzmann constant).
However, the Mg2+-induced increase in Po was suppressed at a relatively low [Ca2+]i (10−5.5–10−6 M). Dwell-time histograms have revealed that addition of Mg2+ mainly increased Po by extending open times at 10−5 M Ca2+ and extending both open and closed times simultaneously at 10−5.5 M Ca2+. Since our data showed that raising the [Ca2+]i from 10−5 to 10−4 M increased Po mainly by shortening the closed time, extension of the closed time at 10−5.5 M Ca2+ would result from the Mg2+-inhibited Ca2+-dependent activation. At a constant Vm, adding Mg2+ enhanced the sigmoidicity of the Po–[Ca2+]i relationship with an increase in the Hill coefficient. These results suggest that the major action of Mg2+ on this channel is to elevate Po by lengthening the open time, while extension of the closed time at a relatively low [Ca2+]i results from a lowering of the sensitivity to Ca2+ of the channel by Mg2+, which causes the increase in the Hill coefficient.
M. Kubokawa and Y. Sohma contributed equally to this work. 相似文献
6.
Oscillatoria anguistissima rapidly adsorbs appreciable amounts of cobalt from the aqueous solutions within 15 min of initial contact with the metal
solution. O. anguistissima showed a high sequestration of cobalt at low equilibrium concentrations, and it followed the Freundlich model of adsorption.
The adsorption is a strongly pH-dependent and temperature-independent phenomenon. The presence of Mg2+ and Ca2+ (100–200 ppm) resulted in decline in Co2+ adsorption capacity of Oscillatoria biomass. Sulphate and nitrate (0.75–10 mM) drastically reduced the extent of Co2+ biosorption. The biosorption of cobalt is an ion-exchange process as the Co2+ binding was accompanied by release of a large amounts of Mg2+ ions. Na2CO3 (1.0 mM) resulted in about 76% desorption of Co2+ from the loaded biomass.
Received: 30 January 1999 / Accepted: 3 March 1999 相似文献
7.
Ana Maria Andia-Waltenbaugh Charlotte A. Tate Naomi Kraus Friedmann 《Molecular and cellular biochemistry》1981,36(3):177-184
Summary Previous work by this and other laboratories has shown that glucagon administration stimulates calcium uptake by subsequently
isolated hepatic mitochondria. This stimulation of hepatic mitochondrial Ca2+ uptake byin vivo administration of glucagon was further characterized in the present report. Maximal stimulation of mitochondrial Ca2+ accumulation was achieved between 6–10 min after the intravenous injection of glucagon into intact rats. Under control conditions,
Ca2+ uptake was inhibited by the presence of Mg2+ in the incubation medium. Glucagon treatment, however, appeared to obliterate the observed inhibition by Mg2+ of mitochondrial Ca2+ uptake. Kinetic experiments revealed the usual sigmoidicity associated with initial velocity curves for mitochondrial calcium
uptake. Glucagon treatment did not alter this sigmoidal relationship. Glucagon treatment significantly increased the Vmax for Ca2+ uptake from 292±22 to 377±34 nmoles Ca2+ /min per mg protein (n=8) but did not affect the K0.5, (6.5–8.6 μM). Since the major kinetic change in mitochondrial Ca2+ uptake evoked by glucagon is an increase in Vmax, the enhancement mechanism is likely to be an increase either in the number of active transport sites available to Ca2+ or in the rate of Ca2+ carrier movement across the mitochondrial membranes. 相似文献
8.
E. M. McLachlan 《Neurophysiology》2007,39(4-5):251-258
The discharge of vasoconstrictor pathways arising in the CNS is largely unmodified as it passes through the sympathetic ganglia
to the vasculature. The underlying synaptic events have been revealed by intracellular recordings from sympathetic paravertebral
ganglion cells in the course of ongoing and reflex activity in anesthetized animals, first made in Skok’s Laboratory in Kyiv
(Ukraine). Each preganglionic neuron diverges to contact a number of post-ganglionic neurons, on each of which several pre-ganglionic
inputs converge. However, only suprathreshold “strong,” or “dominant” synapses are effective in transmitting the CNS signals.
Strong synapses differ from the other subthreshold “weak,” or “accessory” inputs: (a) excitatory synaptic currents are >1
nA in their amplitude, (b) 3 to ≈>30 times more quanta of acetylcholine are released, (c) pre-synaptic Ca2+ entry through channels resistant to all-known antagonists triggers acetylcholine release, and (d) post-synaptic Ca2+ entry boosts and prolongs the nicotinic current. While the majority of postganglionic neurons have only one strong input,
a proportion receives two or, rarely, three such inputs. In cells with multiple strong inputs, an equivalent number of discrete
Ca2+ currents can be evoked at distinct foci electrically distant from the soma, suggesting that each strong input has a unique
dendritic association with a cluster of Ca2+ channels. When strong preganglionic inputs are destroyed, residual weak synapses sprout and rapidly restore the suprathreshold
connections. While much remains to be discovered about how strong synapses are established, their high safety factor ensures
the wide and secure distribution of vasoconstrictor command signals from the CNS.
Neirofiziologiya/Neurophysiology, Vol. 39, Nos. 4/5, pp. 294–301, July–October, 2007. 相似文献
9.
Cefaratti C 《Molecular and cellular biochemistry》2007,295(1-2):241-247
Isolated hepatocytes release 2–3 nmol Mg2+/mg protein or ~10% of the total cellular Mg2+ content within 2 minutes from the addition of agonists that increase cellular cAMP, for example, isoproterenol (ISO). During
Mg2+ release, a quantitatively similar amount of Ca2+ enters the hepatocyte, thus suggesting a stoichiometric exchange ratio of 1 Mg2+:1Ca2+. Calcium induced Mg2+ extrusion is also observed in apical liver plasma membranes (aLPM), in which the process presents the same 1 Mg2+:1Ca2+ exchange ratio. The uptake of Ca2+ for the release of Mg2+ occurs in the absence of significant changes in Δψ as evidenced by electroneutral exchange measurements with a tetraphenylphosphonium
(TPP+) electrode or 3H-TPP+. Collapsing the Δψ by high concentrations of TPP+ or protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) does not inhibit the Ca2+-induced Mg2+ extrusion in cells or aLPM. Further, the process is strictly unidirectional, serving only in Ca2+ uptake and Mg2+ release. These data demonstrate the operation of an electroneutral Ca2+/Mg2+ exchanger which represents a novel pathway for Ca2+ accumulation in liver cells following adrenergic receptor stimulation.
This work was supported by National Institutes of Health Grant HL 18708. 相似文献
10.
Isolated hepatocytes in physiological [Na+]
0
tightly maintain [Mg2+]
i
. Upon β-adrenergic stimulation or in the presence of permeable cAMP, hepatocytes release 5–10% (1–3 mM Mg2+) of their total Mg2+ content. However, isolated basolateral liver plasma membranes (bLPM), release Mg2+ in the presence of [Na+]
o
even in the absence of catecholamine stimulation. The data indicate that a physiological brake for Mg2+ efflux is present in the hepatocyte and is removed upon cellular signaling. In contrast, this regulation “brake” is absent
in purified bLPM thus rendering them fully active. The present study was carried out to reconstruct the missing regulatory
component. Activation of Mg2+ extrusion in intact cells is consistent with cAMP dependent phosphorylation of the transporter or a regulatory protein. Treatment
of bLPM with a non-specific phosphatase such as alkaline phosphatase (AP), decreased Mg2+ efflux by 70% compared to untreated bLPM. When AP-treated bLPM were loaded with protein kinase A (PKA), and stimulated with
permeable cAMP, Mg2+ transport fully recovered. These data suggest that phosphorylation of the Na+/Mg2+ exchanger or a nearby protein activates the Mg2+ transport mechanism in hepatocytes. 相似文献
11.
Kyle V. Lopin Carlos A. Obejero-Paz Stephen W. Jones 《The Journal of membrane biology》2010,235(2):131-143
We explored the ability of a two-site, three-barrier (2S3B) Eyring model to describe recently reported data on current flow
through open CaV3.1 T-type calcium channels, varying Ca2+ and Ba2+ over a wide range (100 nm–110 mm) while recording whole-cell currents over a wide voltage range (−150 mV to +100 mV) from channels stably expressed in HEK
293 cells. Effects on permeation were isolated using instantaneous current–voltage relationships (IIV) after strong, brief
depolarizations to activate channels with minimal inactivation. Most experimental results were reproduced by a 2S3B model.
The model described the IIV relationships, apparent affinities for permeation and block for Ca2+ and Ba2+, and shifts in reversal potential between Ca2+ and Ba2+. The fit to block by 1 mm
\textMg2+\texti {\text{Mg}}^{2+}_{\text{i}} was reasonable, but block by
\textMg2+\texto {\text{Mg}}^{2+}_{\text{o}} was described less well. Surprisingly, fits were comparable with strong ion–ion repulsion, with no repulsion, or with intermediate
values. With weak repulsion, there was a single high-affinity site, with a low-affinity site near the cytoplasmic side of
the pore. With strong repulsion, the net charge of ions in the pore was near +2 over a relatively wide range of concentration
and voltage, suggesting a knockoff mechanism. With strong repulsion, Ba2+ preferred the inner site, while Ca2+ preferred the outer site, potentially explaining faster entry of Ni2+ and other pore blockers when Ba2+ is the charge carrier. 相似文献
12.
Fifteen-year Change in Forest Floor Organic and Element Content and Cycling at the Turkey Lakes Watershed 总被引:11,自引:0,他引:11
To assess the long-term effects of atmospheric deposition on forest floor chemical composition, we took quantitative samplings
of L-(Oi), F-(Oe), and H-(Oa) layers at an old-growth sugar maple–yellow birch stand on a till soil at the Turkey Lakes Watershed
near Lake Superior, Ontario, Canada, in 1981 and 1996. We then assessed these samples for contents of organic matter (OM),
total N, K, Ca, Mg, S, and Na, and exchangeable NH4
+, NO3
−, K+, Ca2+, Mg2+, SO4
2−, and Na+. Over the 15-year period, total OM and element contents remained unchanged, with the exception of N, which increased significantly
from 61.3 kmol/ha in 1981 to 78.4 kmol/ha in 1996. On an area basis, there were significant increases in exchangeable Ca2+ (from 3.8 to 4.6 kmol/ha) and Na+ (from 0.05 to 0.08 kmol/ha) and decreases in exchangeable NH4
+-N (from 1.41 to 0.95 kmol/ha) and SO4
2−-S (from 1.29 to 0.96 kmol/ha). There were no significant differences in average annual litterfall OM, N, Ca, Mg, S or Na
inputs between 1980 and 1985 and between 1992 and 1997. Average annual wet-only SO4
2−-S deposition during 1981–86 was 0.30; during 1992–97, it was 0.21 kmol/ha. Annual wet-only NO3
−-N averaged 0.33 kmol/ha during 1981–86 and was similar during 1992–97. Throughfall was less rich in SO4
2− and Ca2+, Mg2+, and Na+ during 1992–97 than earlier. Throughfall NH4
+ and NO3
− fluxes were unchanged. Efflux of cations from the forest floor reflected reduced throughput of SO4
2−. Overall, the results suggest that in spite of atmospheric inputs, active biological processes—including litter input, fine-root
turnover, and tree uptake—serve to impart stability to the mineral composition of mature sugar maple forest floor.
Received 5 October 1999; accepted 25 October 2000. 相似文献
13.
Yu Ding Jin-Lai Miao Quan-Fu Wang Zhou Zheng Guang-You Li Ji-Chang Jian Zao-He Wu 《Polar Biology》2007,31(1):23-30
A psychrophilic glutathione reductase from Antarctic ice microalgae Chlamydomonas sp. Strain ICE-L was purified by ammonium sulfate fractionation and three steps of chromatography. The yield was up to 25.1%
of total glutathione reductase in the crude enzyme extract. The glutathione reductase activity was characterized by the spectrophotometric
method under different conditions. Purified glutathione reductase was separated by SDS-PAGE, which furnished a homogeneous
band. The native molecular mass of the enzyme was 115 kDa. Apparent Km values for NADPH and NADH (both at 0.5 mmol L−1 oxidized glutathione) were 22.3 and 83.8 μmol L−1, respectively. It was optimally active at pH 7.5, and it was stable from pH 5 to 9. Its optimum temperature was 25°C, with
activity at 0°C 23.5% of the maximum. Its optimum ion strength and optimum Mg2+ were 50–90 and 7.5 mmol L−1, respectively. Ca2+, Mg2+, and cysteine substantially increased the activity of the enzyme but chelating agents, heavy metals (Cd2+, Pb2+, Cu2+, Zn2+, etc.), NADPH, and ADP had significant inhibitory effects. This glutathione reductase can be used to study the adaptation
and mechanism of catalysis of psychrophilic enzymes, and it has a high potential as an environmental biochemical indicator
under extreme conditions. 相似文献
14.
Georgina Rodríguez de Lores Arnaiz Amanda Pellegrino de Iraldi 《Neurochemical research》1997,22(3):293-296
Neuronal ATPases comprise a wide variety of enzymes which are not uniformly distributed in different membrane preparations. Since purified vesicle fractions have Mg2+/Ca2+-ATPase, the purpose of the present study was to know whether such enzyme activities have a preferential concentration in a synaptic vesicle fraction in order to be used as markers for these organelles. Resorting to a procedure developed in this Institute, we fractionated the rat cerebral cortex by differential centrifugation following osmotic shock of a crude mitochondrial fraction and separated a purified synaptic vesicle fraction over discontinuous sucrose gradients. Mg2+/Ca2+-ATPase activities and ultrastructural studies of isolated fractions were carried out. It was observed that similar specific activities for Mg2+/Ca2+-ATPases were found in all fractions studied which contain synaptic vesicles and/or membranes. Although the present results confirm the presence of Mg2+ and Ca2+-ATPase activities in synaptic vesicles preparations, they do not favor the contention that Mg2+/Ca2+-ATPase is a good marker for synaptic vesicles. 相似文献
15.
Density functional theory (DFT) has been applied to study the micro-mechanisms of Al3+ interfering the reactivities of aspartic acid (H2asp) and its biological processes with Mg2+. All the 46 stable conformers of Hasp- and 3 of asp2− have been determined at the B3LYP/6-311++G** level, showing that the 7 most stable conformers of Hasp− all present a very strong and linear O–H···O H-bond between carboxyl and carboxylic acid groups with the bond energy high
up to 162 kJ mol−1. The reaction thermodynamics and micro-mechanism between Al3+ and Hasp− (or asp2−) in aqueous phase have been investigated by the combined application of supramolecular model and polarizable continuum IEFPCM
solvent model, firstly revealing Al3+ interfering in the biological processes of aspartic acid. The substitution thermodynamics and mechanisms of Mg2+ by Al3+ in the biological processes between the species of aspartic acid and Mg2+ in aqueous phase were probed, revealing the facile displacement of Mg2+ by Al3+. These results may provide a reasonable mechanism of Al3+ biological toxicity at the microscopic level. 相似文献
16.
Energy-using non-mitochondrial ATPases were assayed in rat cerebral cortex synaptosomes and synaptosomal subfractions, namely synaptosomal plasma membranes and synaptic vesicles. The following enzyme activities were evaluated: Na+, K+-ATPase; high- and low-affinity Ca2+-ATPase; basal Mg2+-ATPase; Ca2+, Mg2+-ATPase. The evaluations were performed after four week-treatment with saline [controls] or -adrenergic agents (-yohimbine, clonidine), energymetabolism interfering compound (theniloxazine), and oxygen-partial pressure increasing agent (almitrine), in order to define the plasticity and the selective changes in individual ATPases. In rat cerebral cortex, the enzyme adaptation to four-week-treatment with -yohimbine or clonidine was characterized by increase in both high- and low-affinity Ca2+-ATPase activities. The action involves the enzyme form located in the synaptic plasma membranes. The enzyme adaptation to the subchronic treatments with theniloxazine or almitrine was characterized by increase in Na+, K+-ATPase or Mg2+-ATPase activities, respectively. The action involves the enzymatic forms located in the synaptic plasma membranes. Thus, the pharmacodynamic effects of the agents tested should also be related to the changes induced in the activity of some specific synaptosomal nonmitochondrial ATPases. 相似文献
17.
Effect of In Vivo Administration of Naloxone on ATP-ase's Enzyme Systems of Synaptic Plasma Membranes from Rat Cerebral Cortex 总被引:2,自引:0,他引:2
Naloxone is a specific competitive antagonist of morphine, acting on opiate receptors, located on neuronal membranes. The effects of in vivo administration of naloxone on energy-consuming non-mitochondrial ATP-ases were studied in two different types of synaptic plasma membranes from rat cerebral cortex, known to contain a high density of opiate receptors. The enzyme activities of Na+, K+-ATP-ase, Ca2+, Mg2+-ATP-ase and Mg2+-ATP-ase and of acetylcholinesterase (AChE) were evaluated on synaptic plasma membranes obtained from control and treated animals with effective dose of naloxone (12g · kg–1 i.m. 30 minutes). In control (vehicle-treated) animals specific enzyme activities assayed on these two types of synaptic plasma membranes are different, being higher on synaptic plasma membranes of II type than of I type, because the first fraction is more enriched in synaptic plasma membranes. The acute treatment with naloxone produced a significant decrease in Ca2+,Mg2+-ATP-ase activity and an increase in AChE activity, only in synaptic plasma membranes of II type. The decrease of Ca2+,Mg2+-ATP-ase enzymatic activity and the increased AChE activity are related to the interference of the drug on Ca2+ homeostasis in synaptosoplasm, that leads to the activation of calcium-dependent processes, i.e. the extrusion of neurotransmitter. These findings give further evidence that pharmacodynamic characteristics of naloxone are also related to increase [Ca2+]
i
, interfering with enzyme systems (Ca2+,Mg2+-ATP-ase) and that this drug increases acetylcholine catabolism in synaptic plasma membranes of cerebral cortex. 相似文献
18.
In mice kept on a diet with no vitamin B1, the total content of thiamine in the brain decreased, and muscle contractions evoked by stimulation of the nerve in phrenico-diaphragmatic
preparations obtained from such animals became weaker. The measurements were performed in Krebs solution with a decreased
content of Ca2+ and increased concentration of Mg2+; values of the developed force were normalized with respect to those in normal Krebs solution. Thus, B1 hypovitaminosis results in a decrease in the efficacy of neuromuscular synaptic transmission. Some neurological symptoms
typical of a deficiency of vitamin B1 in the organism can be related to this effect.
Neirofiziologiya/Neurophysiology, Vol. 39, Nos. 4/5, pp. 416–418, July–October, 2007. 相似文献
19.
Magnesium Inhibition of Ryanodine-Receptor Calcium Channels: Evidence for Two Independent Mechanisms 总被引:16,自引:0,他引:16
The gating of ryanodine receptor calcium release channels (RyRs) depends on myoplasmic Ca2+ and Mg2+ concentrations. RyRs from skeletal and cardiac muscle are activated by μm Ca2+ and inhibited by mm Ca2+ and Mg2+. 45Ca2+ release from skeletal SR vesicles suggests two mechanisms for Mg2+-inhibition (Meissner, Darling & Eveleth, 1986, Biochemistry
25:236–244). The present study investigates the nature of these mechanisms using measurements of single-channel activity from
cardiac- and skeletal RyRs incorporated into planar lipid bilayers.
Our measurements of Mg2+- and Ca2+-dependent gating kinetics confirm that there are two mechanisms for Mg2+ inhibition (Type I and II inhibition) in skeletal and cardiac RyRs. The mechanisms operate concurrently, are independent
and are associated with different parts of the channel protein. Mg2+ reduces P
o
by competing with Ca2+ for the activation site (Type-I) or binding to more than one, and probably two low affinity inhibition sites which do not
discriminate between Ca2+ and Mg2+ (Type-II). The relative contributions of the two inhibition mechanisms to the total Mg2+ effect depend on cytoplasmic [Ca2+] in such a way that Mg2+ inhibition has the properties of Types-I and II inhibition at low and high [Ca2+] respectively. Both mechanisms are equally important when [Ca2+] = 10 μm in cardiac RyRs or 1 μm in skeletal RyRs. We show that Type-I inhibition is not the sole mechanism responsible for Mg2+ inhibition, as is often assumed, and we discuss the physiological implications of this finding.
Received: 1 January 1996/Revised: 14 November 1996 相似文献
20.
Liang C Xiao W Hao H Xiaoqing L Chao L Lei Z Fashui H 《Biological trace element research》2008,121(3):249-257
Mg2+ in various concentrations was added to purified Rubisco in vitro to gain insight into the mechanism of molecular interactions
between Mg2+ and Rubisco. The enzyme activity assays showed that the reaction between Rubisco and Mg2+ was two order, which means that the enhancement of Rubisco activity was accelerated by low concentration of Mg2+ and slowed by high concentration of Mg2+. The kinetics constant (K
m) and V
max was 1.91 μM and 1.13 μmol CO2 mg−1 protein∙min−1, respectively, at a low concentration of Mg2+, and 3.45 μM and 0.32 μmol CO2∙mg−1 protein∙min−1, respectively, at a high concentration of Mg2+. By UV absorption and fluorescence spectroscopy assays, the Mg2+ was determined to be directly bound to Rubisco; the binding site of Mg2+ to Rubisco was 0.275, the binding constants (K
A) of the binding site were 6.33 × 104 and 5.5 × 104 l·mol−1. Based on the analysis of the circular dichroism (CD) spectra, it was concluded that the binding of Mg2+ did not alter the secondary structure of Rubisco, suggesting that the observed enhancement of Rubisco carboxylase activity
was caused by a subtle structural change in the active site through the formation of the complex with Mg2+. 相似文献