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1.
The self-incompatibility response in Papaver rhoeas is mediated by cytosolic free calcium 总被引:6,自引:1,他引:5
Vernonica E. Franklin-Tong Jon P. Ride Nick D. Read Anthony J. Trewavas F. Christopher H. Franklin 《The Plant journal : for cell and molecular biology》1993,4(1):163-177
The role of Ca2+ signalling during the self-incompatibility (SI) response in Papaver rhoeas L. has been investigated using Ca2+ -sensitive dyes. Pollen tubes were micro-injected with Calcium Green-1 and cytosolic free calcium ([Ca2+ ]i ) imaged using laser scanning confocal microscopy (LSCM). Addition of incompatible stigmatic S-glycoproteins induced a transient increase in the level of [Ca2+ ]i in pollen tubes. In contrast, no rise in [Ca2+ ]i was detectable after addition of either compatible or heat-denatured incompatible stigmatic S-glycoproteins. The elevation of [Ca2+ ]i was followed by the specific inhibition of pollen tube growth in incompatible reactions. It has been shown previously that gene expression in pollen tubes is switched on during an incompatible reaction. Since the [Ca2+ ]i transient appeared to originate from the region where the nuclei are located, Ca2+ may be involved in locally regulating the expression of these genes. The photoactivation of caged Ca2+ to artificially elevate [Ca2+ ]i resulted in the inhibition of pollen tube growth and thus mimicked the SI response. Taken together, the results provide an important link between a transient rise in [Ca2+ ]i and the biological phenomenon of inhibition of pollen tube growth and demonstrate, for the first time, direct evidence that the SI response in P. rhoeas is mediated by [Ca2+ ]i . 相似文献
2.
Effects of Calcium Channel Antagonists on Calcium Entry and Glutamate Release from Cultured Rat Cerebellar Granule Cells 总被引:1,自引:0,他引:1
Abstract: Using a range of Ca2+ channel blockers we have investigated the Ca2+ channel subtypes that mediate the depolarisation-induced elevation of the intracellular free Ca2+ concentration ([Ca2+ ]i ) and glutamate release from cultured rat cerebellar granule cells. ω-Conotoxin-GVIA had little effect on either the transient or plateau phase of the depolarisation-induced [Ca2+ ]i rise or on glutamate release, ruling out a significant role for N-type Ca2+ channels. Nifedipine substantially inhibited the initial transient rise in [Ca2+ ]i and the plateau phase of the [Ca2+ ]i rise and glutamate release, suggesting the involvement of L-type Ca2+ channels. Both ω-agatoxin and ω-conotoxin-MVIIC also inhibited the transient rise in [Ca2+ ]i and glutamate release but not the plateau phase of the [Ca2+ ]i rise. The inhibitions by nifedipine were not increased by coaddition of ω-conotoxin-MVIIC, suggesting overlapping sensitivity to these channel blockers. These data show that glutamate release from granule cells in response to depolarisation with a high KCI level involves Ca2+ currents that are sensitive to nifedipine, ω-agatoxin-IVA, and also ω-conotoxin-MVIIC. The overlapping sensitivity of the channels to these toxins prevents attribution of any of the phases of the [Ca2+ ]i rise or glutamate release to distinct P-, Q-, or O-type Ca2+ currents. 相似文献
3.
Direct Observation of Serotonin 5-HT3 Receptor-Induced Increases in Calcium Levels in Individual Brain Nerve Terminals 总被引:4,自引:1,他引:3
Abstract: Confocal microscopy was used to assess internal calcium level changes in response to presynaptic receptor activation in individual, isolated nerve terminals (synaptosomes) from rat corpus striatum, focusing, in particular, on the serotonin 5-HT3 receptor, a ligand-gated ion channel. The 5-HT3 receptor agonist-induced calcium level changes in individual synaptosomes were compared with responses evoked by K+ depolarization. Using the fluorescent dye fluo-3 to measure relative changes in internal free Ca2+ concentration ([Ca2+ ]i ), K+ -induced depolarization resulted in variable but rapid increases in apparent [Ca2+ ]i among the individual terminals, with some synaptosomes displaying large transient [Ca2+ ]i peaks of varying size (two- to 12-fold over basal levels) followed by an apparent plateau phase, whereas others displayed only a rise to a sustained plateau level of [Ca2+ ]i (two- to 2.5-fold over basal levels). Agonist activation of 5-HT3 receptors induced slow increases in [Ca2+ ]i (rise time, 15–20 s) in a subset (∼5%) of corpus striatal synaptosomes, with the increases (averaging 2.2-fold over basal) being dependent on Ca2+ entry and inhibited by millimolar external Mg2+ . We conclude that significant increases in brain nerve terminal Ca2+ , rivaling that found in response to excitation by depolarization but having distinct kinetic properties, can therefore result from the activation of presynaptic ligand-gated ion channels. 相似文献
4.
Abstract: Nitric oxide has been recognized in recent years as an important mediator of neuronal toxicity, which in many cases involves alterations of the cytoplasmic Ca2+ concentration ([Ca2+ ]i ). In [Ca2+ ]i fluorimetric experiments on cultured hippocampal neurons, the nitric oxide-releasing agent S -nitrosocysteine produced a delayed rise in [Ca2+ ]i over a 20-min exposure, which was accompanied by a progressive slowing of the kinetics of recovery from depolarization-induced [Ca2+ ]i transients. These effects were blocked by oxyhemoglobin and by superoxide dismutase, confirming nitric oxide as the responsible agent, and suggesting that they involved peroxynitrite formation. Similar alterations of [Ca2+ ]i homeostasis were produced by the mitochondrial ATP synthase inhibitor oligomycin, and when an ATP-regenerating system was supplied via the patch pipette in combined whole-cell patch-clamp-[Ca2+ ]i fluorimetry experiments, S -nitrosocysteine had no effect on the resting [Ca2+ ]i or on the recovery kinetics of [Ca2+ ]i transients induced by direct depolarization. We conclude that prolonged exposure to nitric oxide disrupts [Ca2+ ]i homeostasis in hippocampal neurons by impairing Ca2+ removal from the cytoplasm, possibly as a result of ATP depletion. The resulting persistent alterations in [Ca2+ ]i may contribute to the delayed neurotoxicity of nitric oxide. 相似文献
5.
Abstract: Cross talk between two phospholipase C (PLC)-linked receptor signalings was investigated in SK-N-BE(2)C human neuroblastoma cells. Sequential stimulation with two agonists at 5-min intervals was performed to examine the interaction between muscarinic and bradykinin (BK) receptors. Pretreatment of cells with a maximal effective concentration (5 µ M ) of BK did not affect the subsequent carbachol (CCh)-induced [Ca2+ ]i rise, but CCh (1 m M ) pretreatment completely abolished the BK-induced [Ca2+ ]i rise without inhibition of BK-induced inositol 1,4,5-trisphosphate (IP3 ) generation. Thapsigargin (1 µ M ) pretreatment abolished the subsequent BK- and CCh-induced [Ca2+ ]i rise, though it did not affect agonist-induced IP3 generation. However, the addition of atropine at plateau phases of CCh-induced [Ca2+ ]i rise and IP3 production caused a rapid decline to the basal levels and then restored the [Ca2+ ]i rise by BK. Treatment of cells with both CCh and BK at the same time showed additive effects in IP3 production. However, the [Ca2+ ]i rise induced by both agonists in the presence or absence of extracellular Ca2+ was the same as the responses triggered by CCh alone. The results suggest that each receptor or receptor-linked PLC activity is not influenced by pretreatment with the other agonist but IP3 -sensitive Ca2+ stores are shared by signal pathways from both receptors. 相似文献
6.
Abstract: The effects of peroxides were investigated on the membrane potential, intracellular Na+ ([Na+ ]i ) and intracellular Ca2+ ([Ca2+ ]i ) concentrations, and basal glutamate release of synaptosomes. Both H2 O2 and the organic cumene hydroperoxide produced a slow and continuous depolarization, parallel to an increase of [Na+ ]i over an incubation period of 15 min. A steady rise of the [Ca2+ ]i due to peroxides was also observed that was external Ca2+ dependent and detected only at an inwardly directed Ca2+ gradient of the plasma membrane. These changes did not correlate with lipid peroxidation, which was elicited by cumene hydroperoxide but not by H2 O2 . Resting release of glutamate remained unchanged during the first 15 min of incubation in the presence of peroxides. These alterations may indicate early dysfunctions in the sequence of events occurring in the nerve terminals in response to oxidative stress. 相似文献
7.
Abstract: Human NT2-N neurons express Ca2+ -permeable α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid glutamate receptors (AMPA-GluRs) and become vulnerable to excitotoxicity when AMPA-GluR desensitization is blocked with cyclothiazide. Although the initial increase in intracellular Ca2+ levels ([Ca2+ ]i ) was 1.9-fold greater in the presence than in the absence of cyclothiazide, Ca2+ entry via AMPA-GluRs in an early phase of the exposure was not necessary to elicit excitotoxicity in these neurons. Rather, subsequent necrosis was caused by a >40-fold rise in [Na+ ]i , which induced a delayed [Ca2+ ]i rise. Transfer of the neurons to a 5 m M Na+ medium after AMPA-GluR activation accelerated the delayed [Ca2+ ]i rise and intensified excitotoxicity. Low-Na+ medium-enhanced excitotoxicity was partially blocked by amiloride or dizocilpine (MK-801), and completely blocked by removal of extracellular Ca2+ , suggesting that Ca2+ entry by reverse operation of Na+ /Ca2+ exchangers and via NMDA glutamate receptors was responsible for the neuronal death after excessive Na+ loading. Our results serve to emphasize the central role of neuronal Na+ loading in AMPA-GluR-mediated excitotoxicity in human neurons. 相似文献
8.
Abstract: To study how growth factors affect stimulus-secretion coupling pathways, we examined the effects of nerve growth factor (NGF), epidermal growth factor (EGF), and insulin on ATP-induced [Ca2+ ]i rise and dopamine secretion in PC12 cells. After a 4-day incubation of cells, all three factors increased ATP-induced dopamine secretion significantly. We then examined which step of ATP-induced secretion was affected by the growth factors. Cellular levels of dopamine-β-hydroxylase and catecholamines were increased by NGF treatment but were not affected by EGF or insulin. The ATP-induced [Ca2+ ]i rise was also enhanced after growth factor treatment. The EC50 of ATP for inducing [Ca2+ ]i rise and dopamine secretion was increased by NGF treatment but not by treatment with EGF or insulin. Accordingly, the dependence on [Ca2+ ]i of dopamine secretion was increased significantly only in NGF-treated cells. Our results suggest that for EGF- and insulin-treated PC12 cells, the increase in secretion is mainly due to increased potency of ATP in inducing [Ca2+ ]i rise. NGF treatment not only increased the potency of ATP but also decreased the Ca2+ sensitivity of the secretory pathway, which as a result becomes more tightly regulated by changes in [Ca2+ ]i . 相似文献
9.
Timothy J. Meier Dora Y. Ho Travis S. Park Robert M. Sapolsky 《Journal of neurochemistry》1998,71(3):1013-1023
Abstract: Excitatory amino acid overstimulation of neurons can lead to a marked rise in cytoplasmic Ca2+ concentration ([Ca2+ ])i ) and be followed by neuron death from hours to days later. If the rise in [Ca2+ ]i is prevented, either by removing Ca2+ from the extracellular environment or by placing Ca2+ chelators in the cytosol of the stimulated cells, the neurotoxicity associated with excitotoxins can be ameliorated. We have recently shown that neurons infected with a herpes simplex virus amplicon vector expressing cDNA for calbindin D28k responded to hypoglycemia with decreased [Ca2+ ]i and increased survival relative to controls. We now report that vector-infected neurons respond to glutamatergic insults with lower [Ca2+ ]i than controls and with increased survival. Infected neurons exposed to sodium cyanide did not respond with lower [Ca2+ ]i than controls, nor did they demonstrate increased survival postinsult. We examine these results in light of our earlier report and in the context of the potential of vectors like this for neuronal gene therapy. 相似文献
10.
Abstract: The role of the Na+ /Ca2+ exchanger and intracellular nonmitochondrial Ca2+ pool in the regulation of cytosolic free calcium concentration ([Ca2+ ]i ) during catecholamine secretion was investigated. Catecholamine secretion and [Ca2+ ]i were simultaneously monitored in a single chromaffin cell. After high-K+ stimulation, control cells and cells in which the Na+ /Ca2+ exchange activity was inhibited showed similar rates of [Ca2+ ]i elevation. However, the recovery of [Ca2+ ]i to resting levels was slower in the inhibited cells. Inhibition of the exchanger increased the total catecholamine secretion by prolonging the secretion. Inhibition of the Ca2+ pump of the intracellular Ca2+ pool with thapsigargin caused a significant delay in the recovery of [Ca2+ ]i and greatly enhanced the secretory events. These data suggest that both the Na+ /Ca2+ exchanger and the thapsigargin-sensitive Ca2+ pool are important in the regulation of [Ca2+ ]i and, by modulating the time course of secretion, are important in determining the extent of secretion. 相似文献
11.
Carbon dioxide induces increases in guard cell cytosolic free calcium 总被引:10,自引:0,他引:10
Alex A.R. Webb Martin R. McAinsh Terry A. Mansfield Alistair M. Hetherington 《The Plant journal : for cell and molecular biology》1996,9(3):297-304
The hypothesis that increases in cytosolic free calcium ([Ca2+ ]i ) are a component of the CO2 signal transduction pathway in stomatal guard cells of Commelina communis has been investigated. This hypothesis was tested using fura-2 fluorescence ratio photometry to measure changes in guard cell [Ca2+ ]i in response to challenge with 700 µl l−1 CO2 . Elevated CO2 induced increases in guard cell [Ca2+ ]i which were similar to those previously reported in response to abscisic acid. [Ca2+ ]i returned to resting values following removal of the CO2 and further application of CO2 resulted in a second increase in [Ca2+ ]i . This demonstrated that the CO2 -induced increases in [Ca2+ ]i were stimulus dependent. Removal of extracellular calcium both prevented the CO2 -induced increase in [Ca2+ ]i and inhibited the associated reduction in stomatal aperture. These data suggest that Ca2+ acts as a second messenger in the CO2 signal transduction pathway and that an increase in [Ca2+ ]i may be a requirement for the stomatal response to CO2 . 相似文献
12.
Protein Phosphorylation and Calcium Uptake into Rat Forebrain Synaptosomes: Modulation by the σ Ligand, 1,3-Ditolylguanidine 总被引:1,自引:0,他引:1
Paul J. Brent Lynn Herd Heather Saunders Alistair T. R. Sim Peter R. Dunkley 《Journal of neurochemistry》1997,68(5):2201-2211
Abstract: The σ ligand 1,3-di- O -tolylguanidine (DTG) increased basal dynamin and decreased depolarization-stimulated phosphorylation of the synaptosomal protein synapsin Ib without having direct effects on protein kinases or protein phosphatases. DTG dose-dependently decreased the basal cytosolic free Ca2+ concentration ([Ca2+ ]i ) and blocked the depolarization-dependent increases in [Ca2+ ]i . These effects were inhibited by the σ antagonists rimcazole and BMY14802. The nitric oxide donors sodium nitroprusside (SNP) and 8-( p -chlorophenylthio)guanosine-3',5'-cyclic monophosphorothioate decreased basal [Ca2+ ]i and the KCl-evoked rise in [Ca2+ ]i to an extent similar to DTG. SNP, but not DTG, produced a rise in cyclic GMP levels, suggesting that the effect of DTG on [Ca2+ ]i was not mediated via downstream regulation of cyclic GMP levels. DTG increased 45 Ca2+ uptake and efflux under basal conditions and inhibited the 45 Ca2+ uptake induced by depolarization with KCl. The KCl-evoked rise in [Ca2+ ]i was inhibited by ω-conotoxin (ω-CgTx)-GVIA and -MVIIC but not nifedipine and ω-agatoxin-IVA. The effect of DTG on decreasing the KCl-evoked rise in [Ca2+ ]i was additive with ω-CgTx-MVIIC but not with ω-CgTx-GVIA. These data suggest that DTG was producing some of its effects on synapsin I and dynamin phosphorylation and intrasynaptosomal Ca2+ levels via inhibition of N-type Ca2+ channels. 相似文献
13.
Abstract In the present study we compared the intracellular level of free calcium ([Ca2+ ]i ) and monomeric (G)/total (G + F) actin ratio in HeLa cells infected with diffuse (DAEC) and localised adherent Escherichia coli (LAEC). The level of [Ca2+ ]i was increased in both DAEC- and LAEC-infected HeLa cells. However, studies with EGTA- and dantrolene-treated cells and also suspension of cells in Ca2+ -free buffer suggested that the rise of [Ca2+ ]i in DAEC-infected cells was due to the influx of Ca2+ from extracellular medium, whereas Ca2+ mobilisation from the intracellular stores was responsible for the enhancement of [Ca2+ ]i in LAEC-infected cells. It was also evident that the infection of HeLa cells with DAEC and LAEC caused alteration of G / G + F actin ratio as compared to that of control cells. The ratio was much lower in LAEC-infected cells than that of DAEC-infected ones. Moreover, cytochalasin B inhibited both DAEC and LAEC invasion to HeLa cells, suggesting further the role of microfilaments in the invasion process. 相似文献
14.
Abstract: Nitric oxide (NO) has been shown to be an important mediator in several forms of neurotoxicity. We previously reported that NO alters intracellular Ca2+ concentration ([Ca2+ ]i ) homeostasis in cultured hippocampal neurons during 20-min exposures. In this study, we examine the relationship between late alterations of [Ca2+ ]i homeostasis and the delayed toxicity produced by NO. The NO-releasing agent S -nitrosocysteine (SNOC; 300 µ M ) reduced survival by about one half 1 day after 20-min exposures, as did other NO-releasing agents. SNOC also was found to produce prolonged elevations of [Ca2+ ]i , persisting at 2 and 6 h. Hemoglobin, a scavenger of NO, blocked both the late [Ca2+ ]i elevation and the delayed toxicity of SNOC. Removal of extracellular Ca2+ during the 20-min SNOC treatment failed to prevent the late [Ca2+ ]i elevations and did not prevent the delayed toxicity, but removal of extracellular Ca2+ for the 6 h after exposure as well blocked most of the toxicity. Western blots showed that SNOC exposure resulted in an increased proteolytic breakdown of the structural protein spectrin, generating a fragment with immunoreactivity suggesting activity of the Ca2+ -activated protease calpain. The spectrin breakdown and the toxicity of SNOC were inhibited by treatment with calpain antagonists. We conclude that exposures to toxic levels of NO cause prolonged disruption of [Ca2+ ]i homeostatic mechanisms, and that the resulting persistent [Ca2+ ]i elevations contribute to the delayed neurotoxicity of NO. 相似文献
15.
Paul Morley Paul MacPherson James F. Whitfield †Eric W. Harris Michael W. McBurney 《Journal of neurochemistry》1995,65(3):1093-1099
Abstract: Retinoic acid-treated murine P19 embryonal carcinoma cells differentiate into cells with neuronal morphology that display typical neuronal markers. In this study, the presence of glutamate receptors linked to Ca2+ -signaling mechanisms on these neurons was demonstrated by testing the effects of glutamate agonists and antagonists on the intracellular calcium ion concentration ([Ca2+ ]i ). Glutamate (1 m M ) induced either sustained or transient increases in [Ca2+ ]i . The sustained glutamate-induced increase in [Ca2+ ]i was mimicked by NMDA (40 µ M ). The NMDA-triggered [Ca2+ ]i response was abolished by incubating the cells in Ca2+ -free medium or by pretreating them with Mg2+ (2 m M ) or MK-801 (0.1 µ M ). These responses were unaffected by the non-NMDA antagonist CNQX (10 µ M ), but they required glycine (3–30 µ M ). Kainate (40 µ M ) and AMPA (40 µ M ) did not affect [Ca2+ ]i . Without external Ca2+ , glutamate triggered transient, sometimes oscillating, increases in [Ca2+ ]i . These responses were mimicked by the metabotropic agonist trans -(1 S ,3 R )-1-amino-1,3-cyclopentanedicarboxylic acid (300 µ M ). These results suggest that neurons derived from P19 embryonal carcinoma cells have NMDA and metabotropic, but not AMPA/kainate receptors, which are linked to Ca2+ -signaling mechanisms. These cells could provide a consistent and reproducible model with which to study neuronal differentiation, neurotoxicity, and glutamate receptor-signaling mechanisms. 相似文献
16.
Kari R. Hoyt Sunita Rajdev Cheryl L. Fattman Ian J. Reynolds 《Journal of neurochemistry》1995,64(5):2049-2056
Abstract: We investigated the modulation of (±)-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-induced increases in intracellular free Ca2+ ([Ca2+ ]i ) and intracellular free Mg2+ ([Mg2+ ]i ) by cyclothiazide and GYKI 52466 using microspectrofluorimetry in single cultured rat brain neurons. AMPA-induced changes in [Ca2+ ]i were increased by 0.3–100 µ M cyclothiazide, with an EC50 value of 2.40 µ M and a maximum potentiation of 428% of control values. [Ca2+ ]i responses to glutamate in the presence of N -methyl- d -aspartate (NMDA) receptor antagonists were also potentiated by 10 µ M cyclothiazide. The response to NMDA was not affected, demonstrating specificity of cyclothiazide for non-NMDA receptors. Almost all neurons responded with an increase in [Ca2+ ]i to both kainate and AMPA in the absence of extracellular Na+ , and these Na+ -free responses were also potentiated by cyclothiazide. GYKI 52466 inhibited responses to AMPA with an IC50 value of 12.0 µ M . Ten micromolar cyclothiazide significantly decreased the potency of GYKI 52466. However, the magnitude of this decrease in potency was not consistent with a competitive interaction between the two ligands. Cyclothiazide also potentiated AMPA- and glutamate-induced increases in [Mg2+ ]i . These results are consistent with the ability of cyclothiazide to decrease desensitization of non-NMDA glutamate receptors and may provide the basis for the increase in non-NMDA receptor-mediated excitotoxicity produced by cyclothiazide. 相似文献
17.
Shei-Ying Hu Shu-Ling Song Mei-Ying Ho Sheau-Huei Chueh 《Journal of neurochemistry》1997,68(2):846-854
Abstract: Prior treatment of NG108-15 cells with phosphatase inhibitors including okadaic acid and calyculin A inhibited the elevation of cytosolic Ca2+ concentration ([Ca2+ ]i ) induced by bradykinin by ∼63%. This inhibition was dependent on the concentration of okadaic acid with an IC50 of 0.15 n M . Okadaic acid treatment only lowered the maximal response of [Ca2+ ]i increase and had no effect on the EC50 value for bradykinin regardless of the presence of extracellular Ca2+ . Neither the capacity of 45 Ca2+ accumulation within intracellular nonmitochondrial Ca2+ stores nor the magnitude of [Ca2+ ]i increase induced by thapsigargin was reduced by the treatment of okadaic acid. In contrast, the same phosphatase inhibitor treatment inhibited the bradykinin-evoked inositol 1,4,5-trisphosphate (IP3 ) generation, the Mn2+ influx, and the capacity of mitochondrial Ca2+ accumulation. Furthermore, the sensitivity of IP3 in the Ca2+ release was suppressed by okadaic acid pretreatment. Our results suggest that the reduction of bradykinin-induced [Ca2+ ]i rise by the promotion of protein phosphorylation was attributed to the reduced activity of phospholipase C, the decreased sensitivity to IP3 , and the slowed rate of Ca2+ influx. Thus, phosphorylation plays a role in bradykinin-sensitive Ca2+ signaling cascade in NG108-15 cells. 相似文献
18.
Ale Neuwirth Dalibor KodríK Heiner Birkenbeil Frantiek Sehnal 《Physiological Entomology》2005,30(3):270-277
Abstract. Secretion of ecdysteroids by the prothoracic glands of the migratory locust, Locusta migratoria L., is enhanced in vitro by tris(hydroxymethyl)aminomethane (tris) in a dose-dependent manner. Glands from larvae on the second day of the penultimate stadium are most sensitive. This action of tris depends on the uptake of calcium; increased production of ecdysteroid does not occur in the presence of cadmium, verapamil or TMB-8, or in calcium-free media. The concentration of unbound Ca2+ , [Ca2+ ]i , in the cytoplasm is measured with the aid of FURA 2/AM. Tris causes a rise of [Ca2+ ]i that is fully suppressed by lanthanum and partially by nitrendipine. Two antagonists of IP3 receptors elicit mutually opposite effects: heparin blocks, whereas 2-APB accelerates, the rise in [Ca2+ ]i . Ryanodine exerts only a slight effect. It is proposed that tris activates locust prothoracic glands in a Ca2+ -dependent manner that exhibits many similarities to the transduction pathway of prothoracicotropic hormone. 相似文献
19.
Katsuaki Hoshino Takeshi Shimizu Yutaka Sendai Tatsuo Harumi Norio Suzuki 《Development, growth & differentiation》1992,34(4):403-411
We examined the effects of two egg jelly components, a fucose sulfate glycoconjugate (FSG) and sperm-activating peptide I (SAP-I: Gly-Phe-Asp-Leu-Asn-Gly-Gly-Gly-Val-Gly), on the intracellular pH (pHi ) and Ca2+ ([Ca2+ ]i ) of spermatozoa of the sea urchin Hemicentrotus pulcherrimus . FSG and/or SAP-I induced elevations of [Ca2+ ]; and pHi in the spermatozoa at pH 8.0. At pH 8.0, a second addition of FSG did not induced further elevation of the [Ca2+ ]i or pHi of spermatozoa treated with FSG, but addition or FSG after SAP-I or of SAP-I after FSG induced further increases of [Ca2+ ]i and pHi , At pH 6.6, FSG and/or SAP-I did not induce significant elevation of the [Ca2+ ]i , although SAP-I elevated the pHi , its half-maximal effective concentration being 10 to 100 pM. At pH 8.0, tetraethyl-ammonium, a voltage-sensitive K+ -channel blocker, inhibited induction of the acrosome reaction and elevations of [Ca2+ ]i and pHi by FSG, but did not affect those by SAP-I. These results suggest that FSG and SAP-I activate different Ca2+ and H+ transport systems. 相似文献
20.
The Metabotropic Glutamate Receptor mGluR5 Induces Calcium Oscillations in Cultured Astrocytes via Protein Kinase C Phosphorylation 总被引:6,自引:3,他引:3
Kiyoshi Nakahara Masamichi Okada Shigetada Nakanishi 《Journal of neurochemistry》1997,69(4):1467-1475
Abstract: The metabotropic glutamate receptor mGluR5, but not the closely related mGluR1, is expressed in cultured astrocytes, and this expression is up-regulated by specific growth factors. We investigated the capability and underlying mechanisms of mGluR5 to induce oscillatory responses of intracellular calcium concentration ([Ca2+ ]i ) in cultured rat astrocytes. Single-cell [Ca2+ ]i recordings indicated that an mGluR-selective agonist, (1 S ,3 R )-1-aminocyclopentane-1,3-dicarboxylate (1 S ,3 R -ACPD), elicits [Ca2+ ]i oscillations in good agreement with the growth factor-induced up-regulation of mGluR5 in cultured astrocytes. A protein kinase C (PKC) inhibitor, bisindolylmaleimide I, converted a 1 S ,3 R -ACPD-mediated oscillatory response into a nonoscillatory response. In addition, the PKC activator phorbol 12-myristate 13-acetate completely abolished the [Ca2+ ]i increase. These and other pharmacological properties of 1 S ,3 R -ACPD-induced [Ca2+ ]i oscillations correlate well with those of the cloned mGluR5 characterized in heterologous expression systems. Furthermore, the potential involvement of protein phosphatases in [Ca2+ ]i oscillations is suggested. The present study demonstrates that mGluR5 is capable of inducing [Ca2+ ]i oscillations in cultured astrocytes and that phosphorylation/dephosphorylation of mGluR5 is critical in [Ca2+ ]i oscillations, analogous to the cloned mGluR5 expressed in heterologous cell lines. 相似文献