共查询到20条相似文献,搜索用时 15 毫秒
1.
Vernonica E. Franklin-Tong Jon P. Ride F. Christopher H. Franklin 《The Plant journal : for cell and molecular biology》1995,8(2):299-307
Evidence for Ca2+ signalling in pollen during the self-incompatibility (SI) response in Papaver rhoeas L. has been presented previously. However, it was not known whether the S-protein alone could act as an elicitor of the response or whether the presence of other stigmatic components was required, since relatively crude stigmatic extracts had been used. The S 1 gene has since been cloned and its product expressed in Escherichia coli has been shown to exhibit biological activity. In this paper it is reported that the recombinant protein (S1 e) elicits a transient rise in [Ca2+ ]i in incompatible pollen. The Ca2+ signal appears indistinguishable from that elicited by S-gene products partially purified from plant extracts in terms of both its timing and spatial distribution. Pollen tube growth is arrested directly after the rise in [Ca2+ ]i .
The results provide direct evidence that the S-protein alone acts as an elicitor which triggers the Ca2+ signal for the pollen SI response. In addition, it is now clear that the recombinant S-protein does not require several post-translational processing events which take place in the plant to act as an elicitor. With respect to the spatial distribution of the Ca2+ transient, data are presented which correlate the localized rise in intracellular Ca2+ ([Ca2+ ]i ) with the 'nuclear complex' and the endoplasmic reticulum which is associated with this region. 相似文献
The results provide direct evidence that the S-protein alone acts as an elicitor which triggers the Ca
2.
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
3.
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
4.
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
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: 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
7.
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
8.
ILSE FOISSNER 《The New phytologist》1998,139(3):449-458
Ca2+ was localized in chemically injured internodal cells of the characean alga Nitella flexilis (L.) Ag. using alizarin red and antimonate precipitation. The presence of Ca2+ in the antimonate precipitates was verified by X-ray analysis and EGTA chelation. Callose-containing amorphous wound walls were induced by 0·1 m m chlortetracycline (CTC) and cellulosic fibrillar wound walls were induced by 50 m m CaCl2 . Numerous precipitates were found in the amorphous wound walls and in the adjacent cytoplasm. Precipitates were mainly localized in single membrane-bound cisternae, probably of the endoplasmic reticulum, which accumulate at the wound and become a component of the amorphous wound wall via membrane fusion. In fibrillar wound walls, which do not contain membranous residues, precipitate density was significantly lower and similar to that in the secondary cell wall.
The data suggest that the high Ca2+ content of amorphous wound walls is due to incorporation of cytoplasmic Ca2+ stores. The possible function of amorphous wound walls in maintaining cellular Ca2+ homeostasis is discussed. 相似文献
The data suggest that the high Ca
9.
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
10.
† Hitoshi Morikawa †Kazuhiko Fukuda †Shigehisa Kato †Kenjiro Mori Haruhiro Higashida 《Journal of neurochemistry》1995,65(3):1403-1406
Abstract: Voltage-dependent Ca2+ currents were measured in NG108-15 neuroblastoma × glioma hybrid cells transformed to express the rat μ-opioid receptor by the whole-cell configuration of the patch-clamp technique with Ba2+ as charge carrier. A μ-opioid receptor-selective agonist, [ d -Ala2 , N -Me-Phe4 ,Gly5 -ol]enkephalin caused significant inhibition of voltage-dependent Ca2+ currents in μ-receptor-transformed NG108-15 cells but not in nontransfected or vector-transformed control cells. On the other hand, a δ-opioid receptor-selective agonist, [ d -penicillamine2 , d -penicillamine5 ]enkephalin, induced inhibition of voltage-dependent Ca2+ currents in both control and μ-receptor-transformed cells, which is mediated by the δ-opioid receptor expressed endogenously in NG108-15 cells. The inhibition of voltage-dependent Ca2+ currents induced by [ d -Ala2 , N -Me-Phe4 ,Gly5 -ol]enkephalin and [ d -penicillamine2 , d -penicillamine5 ]enkephalin was reduced by pretreatment of the cells with pertussis toxin or ω-conotoxin GVIA. These results indicate that the μ-opioid receptor expressed from cDNA functionally couples with ω-conotoxin-sensitive N-type Ca2+ channels through the action of pertussis toxin-sensitive G proteins in NG108-15 cells. 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.
The protein kinase inhibitor K-252a induces a rapid, transient decrease of extracellular pH and [K+ ], and a concomitant increase in extracellular [Ca2+ ] in suspensions of cultured parsley cells. These effects are subsequently reversed. As with K-252a, fusicoccin also induces similar changes in pH and extracellular [Ca2+ ], but reversion does not occur. Acidification by HCI also leads to an increase in external [Ca2+ ], suggesting that the changes in extracellular [Ca2+ ] are mainly due to a pH-dependent displacement of Ca2+ ionically bound to the cell wall. The artificial acidification by HCI is rapidly followed by cell-mediated alkalinization, a process associated with K2 release and rebinding of Ca2+ . Any change in external pH or [K+ ] induced by K-252a, fusicoccin, or HCI is followed by an uptake of 45 Ca2+ into cellular pools. The results show that K-252a may be a valuable tool for studying the complex regulation of ion transport which may involve changes in the phosphorylation of unknown proteins. 相似文献
13.
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
14.
Peter B. Simpson R. A. John Challiss Stefan R. Nahorski 《Journal of neurochemistry》1993,61(2):760-763
Abstract: The [Ca2+ ]1 of cerebellar granule cells can be increased in a biphasic manner by addition of NMDA or by depolarization (induced by elevating the extracellular K+ level), which both activate Ca2+ influx. The possibility that these stimuli activate Ca2+ -induced Ca2+ release was investigated using granule cells loaded with fura 2-AM. Dantrolene, perfused onto groups of cells during the sustained plateau phase of the [Ca2+ ]1 response to K+ or NMDA, was found to reduce the response to both agents in a concentration-dependent manner. Preincubation with thapsigargm (10 μ M ) substantially reduced the plateau phase of the [Ca2+ ], response to K+ and both the peak and plateau phases of the NMDA response. Preincubation with ryanodine (10 μ M ) also reduced both the K+ -evoked plateau response and both phases of the NMDA response. Neither had a consistent effect on the peak response to K+ . The effects of thapsigargin and ryanodine on the NMDA response were partially additive. These results demonstrate that in cerebellar granule cells a major component of both K+ - and NMDA-induced elevation of [Ca2+ ]1 appears to be due to release from intracellular stores. The partial additivity of the effects of thapsigargin and ryanodine suggests that these agents affect two overlapping but nonidentical Ca2+ pools. 相似文献
15.
† Mark P. Mattson ‡Mark A. Lovell Katsutoshi Furukawa §William R. Markesbery 《Journal of neurochemistry》1995,65(4):1740-1751
Abstract: Exposure of cultured rat hippocampal neurons to glutamate resulted in accumulation of cellular peroxides (measured using the dye 2,7-dichlorofluorescein). Peroxide accumulation was prevented by an N -methyl- d -aspartate (NMDA) receptor antagonist and by removal of extracellular Ca2+ , indicating the involvement of NMDA receptor-induced Ca2+ influx in peroxide accumulation. Glutamate-induced reactive oxygen species contributed to loss of Ca2+ homeostasis and excitotoxic injury because antioxidants (vitamin E, propyl gallate, and N-tert -butyl-α-phenylnitrone) suppressed glutamate-induced elevation of intracellular Ca2+ concentration ([Ca2+ ]i ) and cell death. Basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF), but not ciliary neurotrophic factor, each suppressed accumulation of peroxides induced by glutamate and protected neurons against excitotoxicity. bFGF, NGF, and BDNF each increased (to varying degrees) activity levels of superoxide dismutases and glutathione reductase. NGF increased catalase activity, and BDNF increased glutathione peroxidase activity. The ability of the neurotrophic factors to suppress glutamate toxicity and glutamate-induced peroxide accumulation was attenuated by the tyrosine kinase inhibitor genistein, indicating the requirement for tyrosine phosphorylation in the neuroprotective signal transduction mechanism. The data suggest that glutamate toxicity involves peroxide production, which contributes to loss of Ca2+ homeostasis, and that induction of antioxidant defense systems is a mechanism underlying the [Ca2+ ]i -stabilizing and excitoprotective actions of neurotrophic factors. 相似文献
16.
Yasuyuki Kamata Masatoshi Mita Akiko Fujiwara Tadashi Tojo Jiro Takano Akira Ide Ikuo Yasumasu 《Development, growth & differentiation》1997,39(4):419-428
In sea urchin eggs activated by sperm, A23187 or melittin, BPB (4-bromophenacyl bromide, a phospholipase A2 inhibitor) blocked fertilization envelope formation and transient CN− -insensitive respiration in a concentration-dependent manner. BPB had virtually no effect on the increase in [Ca2+ ]i , (cytosolic Ca2+ level), the activity of phosphorylase a and the rate of protein synthesis, as well as acid production and augmentation of CN− -sensitive respiration. BPB also inhibited fertilization envelope formation and augmentation of CN− -insensitive respiration induced by melittin. Melittin, known to be an activator of phospholipase A2 , induced the envelope formation, acid production, augmentation of CN− -insensitive and sensitive respiration, but did not cause any increase in [Ca2+ ]i , the phosphorylase a activity and the rate of protein synthesis. An activation of phospholipase A2 induced by Ca2+ or melittin seems to result in cortical vesicle discharge and production of fatty acids, which are to be utilized in CN− -insensitive lipid peroxidase reactions. Activation of other examined cell functions in eggs activated by sperm or A23187, probably results from Ca2+ -triggered sequential reactions other than Ca2+ -caused activation of phospholipase A2 . 相似文献
17.
Increases in cytosolic free Ca2+ ([Ca2+ ]cyt ) are common to many stress-activated signalling pathways, including the response to saline environments. We have investigated the nature of NaCl-induced [Ca2+ ]cyt signals in whole Arabidopsis thaliana seedlings using aequorin. We found that NaCl-induced increases in [Ca2+ ]cyt are heterogeneous and mainly restricted to the root. Both the concentration of NaCl and the composition of the solution bathing the root have profound effects on the magnitude and dynamics of NaCl-induced increases in [Ca2+ ]cyt . Alteration of external K+ concentration caused changes in the temporal and spatial pattern of [Ca2+ ]cyt increase, providing evidence for Na+ -induced Ca2+ influx across the plasma membrane. The effects of various pharmacological agents on NaCl-induced increases in [Ca2+ ]cyt indicate that NaCl may induce influx of Ca2+ through both plasma membrane and intracellular Ca2+ -permeable channels. Analysis of spatiotemporal [Ca2+ ]cyt dynamics using photon-counting imaging revealed additional levels of complexity in the [Ca2+ ]cyt signal that may reflect the oscillatory nature of NaCl-induced changes in single cells. 相似文献
18.
Tadashi Tojo Yasuyuki Kamata Akiko Fujiwara Ikuo Yasumasu 《Development, growth & differentiation》1995,37(1):49-56
In sea urchin eggs, 10 μg/mL melittin was found to induce fertilization envelope formation without any increase in [Ca2+ ]i (the intracellular free Ca2+ level). On the other hand, 10 μmol/L Br-A23187 and 100 μg/mL SDS induced fertilization envelope formation associated with [Ca2+ ]i increase. If EGTA was injected into eggs to make an intracellular concentration of 2 mmol/L, [Ca2+ ]i became quite low and was not altered by melittin, or by Br-A23187 and SDS. In eggs containing EGTA, fertilization envelope formation was induced by melittin even in Ca2+ -free artificial sea water, but not by Br-A23187 or SDS. Thus [Ca2+ ]i is essential for induction of a fertilization envelope in sea urchin eggs by Br-A23187 or SDS but not by melittin. Melittin probably activates some Ca2+ -independent reaction downstream of Ca2+ -dependent reactions in a sequential reaction system that finally results in fertilization envelope formation. 相似文献
19.
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
20.
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