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1.
Tonoplast Action Potential of Characeae 总被引:2,自引:0,他引:2
The plasmalemma action potential was found to be indispensableto the production of the tonoplast action potential. In a solutionlacking Ca2+ and containing other divalent cations such as Ba2+,Mg2+ or Mn2+, the plasmalemma excited in Nitella but did notin Chara. In Nitella, however, both the tonoplast action potentialand EC-coupling were abolished due to depletion of Ca2+ fromthe external medium. Ca2+ ions injected into the cytoplasmiclayer caused a transient change in both plasmalemma and tonoplastpotentials. These results suggest that a transient rise in Ca2+concentration during excitation of the plasmalemma may triggerthe tonoplast action potential. (Received February 14, 1986; Accepted August 29, 1986) 相似文献
2.
Cytoplasmic drops were prepared from internodal cells of thebrackish Characeae Lamprothamnium succinctum. Applying the patch-clamptechnique to single drops covered with tonoplast, we demonstratedthe presence of Ca2+-regulated K+ channels in the tonoplast.In a cell-attached mode, the selectivity of such channels forK+ was about 50 times that for Na+. This channel showed a tendencyto rectify in an outward direction. In the negative region ofthe pipette voltage, the conductance of this channel was 50pS, while it was 100 pS in the positive voltage region. Whenthe pipette voltage was increased above 50 mV, two conductancelevels were found in the cell-attached mode as well as in theexcised patch (cytoplasmic-side-out patch), which was obtainedby pulling the patch pipette from the cytoplasmic drop underconditions of low levels of Ca2+. Using the excised patch, wecontrolled the level of Ca2+ on the cytoplasmic side of thechannels. At a low level of Ca2+ (pCa=8) on the cytoplasmicside, the open frequency was very low and the opening time wasshort. An increase in Ca2+ on the cytoplasmic side (pCa = 5)increased both the frequency and the duration of opening. However,the conductance of the channels did not change. This regulationby Ca2+ of the K+ channels was reversible, that is, additionof EGTA on the cytoplasmic side inactivated the channels. Thepresent study demonstrates a direct action of Ca2+ on the K+channels. The physiological role of the K+ channel in the regulationof turgor in Lamprothamnium is discussed. (Received January 9, 1989; Accepted March 8, 1989) 相似文献
3.
Using permeabilized characean cells in which the ionic conditionsat the cytoplasmic side of the tonoplast are easily controlled,effects of Ca2+ ion on tonoplast potential were examined. Whenthe cell was treated with 1 µM Ca2+, the tonoplast potential(EM became positive in a complicated manner in Chara corallinawhile it simply became negative in Nitella axilliformis. Whenthe cell was treated with 9-antracenecarboxylic acid, a Cl-channelinhibitor, Em became more negative and the response of Em toCa2+ was significantly suppressed. It is suggested that Ca2+activates Cl-channel at a low concentration and inactivatesat a higher one in C. corallina while it simply inactivate Cl-channelin N. axilliformis.
1Present address: Biological Laboratory, The University of theAir, Wakaba 2-11, Wakaba, 260 Japan. (Received August 22, 1988; Accepted December 26, 1988) 相似文献
4.
The turgor regulation induced by hypotonic treatment (hypotonicturgor regulation) in the brackish-water alga Lamprothamniumsuccinctum is accompanied by a transient increase in the electricalconductance of the membrane, membrane depolarization and a transientincrease in the cytoplasmic concentration of free Ca2+ ([Ca2+([Ca2+]c) (Okazaki and Tazawa 1990). In the present study, weloaded a Ca2+-chelating agent, EGTA, into the cytoplasm by mechanicalinjection in order to suppress the increase in [Ca2+]c thatoccurs during the hypotonic turgor regulation. The rate of thecytoplasmic streaming was taken as an indirect indicator of[Ca2+]c, since cytoplasmic streaming has been shown to be inhibitedby high [Ca2+]c in Lamprothamnium cells. The lag time for theinhibition of the cytoplasmic streaming upon hypotonic treatmentwas significantly prolonged in EGTA-loaded cells as comparedto that in intact cells. This result indicates that the loadedcytoplasmic EGTA functioned as a buffer of Ca2+ to retard theincrease in [Ca2+]c. It took a longer time for the membraneconductance to reach the peak value in EGTA-loaded cells thanin intact cells. Membrane depolarization was affected to aninsignificant extent by the cytoplasmic EGTA. The regulationof turgor pressure itself was partially inhibited. These resultsstrongly support the idea that the net efflux of ions that occursduring the recovery from hy-potonically induced changes in turgorpressure is controlled by [Ca2+]c. (Received August 22, 1990; Accepted December 6, 1990) 相似文献
5.
Cytoplasmic drops covered with the tonoplast were prepared frominternodal cells of Nitellopsis grown in fresh water. Applyingthe patch-clamp technique and the microinjection technique tosuch drops, we characterized the ion channels in the tonoplast.Both in cell-free patches and in the cytoplasmic-drop-attachedpatches, the tonoplast K+ channel was identified. The permeabilityratio between Na+ and K+ was calculated to be 0.2. This channelwould provide a molecular basis for the Na+/K+ exchange at thetonoplast. In cell-free patches, the K+channel was not activatedby Ca2+. However, in the case of attached patches, microinjectionof Ca2+ into a drop activated the K+ channel with a lag of afew seconds, suggesting that some cytoplasmic factor(s) maymediate the activation of the K+ channel by Ca2+. The conductanceof this channel was not changed by cytoplasmic Ca2+, but theprobability of opening increased markedly. In addition to theK+ channel, a second type of channel was also identified incell-free patches. This channel may be the Cl channel.
3 Present address: Department of Insect Physiology and Behavior,National Institute of Sericultural and Entomological Science,Tsukuba, Ibaraki, 305 Japan (Received August 6, 1990; Accepted December 6, 1990) 相似文献
6.
Sphingosylphosphorylcholine stimulates mitogen-activated protein kinase via a Ca2+-dependent pathway 总被引:1,自引:0,他引:1
In cultured porcine aortic smooth muscle cells,sphingosylphosphorylcholine (SPC), ATP, or bradykinin (BK) induced arapid dose-dependent increase in the cytosolicCa2+ concentration([Ca2+]i)and also stimulated inositol 1,4,5-trisphosphate(IP3) generation. Pretreatmentof cells with pertussis toxin blocked the SPC-induced IP3 generation and[Ca2+]iincrease but had no effect on the action of ATP or BK. In addition, SPCstimulated the mitogen-activated protein kinase (MAPK) and increasedDNA synthesis, whereas neither ATP nor BK produced such effects. Boththe SPC-induced MAPK activation and DNA synthesis were pertussis toxinsensitive. SPC-induced MAPK activation was blocked by treatment ofcells with the phospholipase C inhibitor, U-73122, or the intracellularCa2+-ATPase inhibitor,thapsigargin, but not by removal of extracellular Ca2+. Lysophosphatidic acidinduced cellular responses similar to SPC in a pertussistoxin-sensitive manner in terms of[Ca2+]iincrease, IP3 generation, MAPKactivation, and DNA synthesis. Platelet-derived growth factor (PDGF)also induced a[Ca2+]iincrease, MAPK activation, and DNA synthesis in the same cells; however, the PDGF-induced MAPK activation was not sensitive to pertussis toxin and changes in[Ca2+]i.SPC-induced MAPK activation was inhibited by pretreatment of cells withstaurosporine, W-7, or calmidazolium. Our results suggest that, inporcine aortic smooth muscle cells, MAPK is not activated by theincrease in[Ca2+]iunless a pertussis toxin-sensitive G protein is simultaneously stimulated, indicating the role ofCa2+ in pertussis toxin-sensitiveG protein-mediated MAPK activation. 相似文献
7.
Summary The origins of the two peaks of the action potential inNitella flexilis were analyzed by inserting two microelectrodes. one into the vacuole and the other into the cytoplasm. It was unequivocally demonstrated that the rapid first peak was generated at the plasmalemma and the slow second peak at the tonoplast. MnCl2 applied in the external medium abolished the second, tonoplast, peak but not the first, plasmalemma, peak, MnCl2 also inhibited the cessation of the cytoplasmic streaming accompanying the action potential. CaCl2 added in MnCl2-containing medium recovered generation of the tonoplast action potential and the streaming cessation. Since it has been established that the cessation of cytoplasmic streaming on membrane excitation is caused by an increase in cytoplasmic free Ca2– (Williamson, R.E., Ashley, C.C., 1982.Nature (London)
296:647–651: Tominaga, Y., Shimmen, T., Tazawa, M., 1983,Protoplasma
116:75–77), it is suggested that the tonoplast action potential is also induced by an increase in cytoplasmic Ca2+ resulting from the plasmalemma excitation. When vacuolar Cl was replaced with SO
4
2
by vacuolar perfusion, the polarity of the second, slow peak was reversed from vacuolar positive to vacuolar negative with respect to the cytoplasm, supporting the previous report that the tonoplast action potential is caused by increase in Cl permeability (Kikuyama, M., Tazawa, M., 1976.J. Membrane Biol.29:95–110). 相似文献
8.
In response to hypotonic treatment internodal cells of the brackishwater Characeae Lamprothamnium regulate turgor pressure by releasingK+ and Cl, accompanying membrane depolarization and atransient increase in membrane electrical conductance (Okazakiet al. 1984b). The hypothesis that a transient increase in cytoplasmicfree Ca2+ concentration ([Ca2+]c) caused by hypotonic treatmenttriggers release of K+ and Cl from the cell (Okazakiand Tazawa 1986a, b, c) was tested using tonoplast-removed cells.These cells did not regulate turgor pressure. The plasmalemmaconductance remained almost constant for a change in the intracellularfree Ca2+ concentration ([Ca2+],) from 106 to 102mol?m3. The results suggest that some cytoplasmic Ca2+-sensitizingsoluble components, which work as mediators to activate K+ and/orCl channels in the plasmalemma and/or the tonoplast,were lost after desintegration of the tonoplast. The plasmalemmapotential was depolarized under high [Ca2+]i. However, no membranedepolarization was observed upon hypotonic treatment. Sincemembrane depolarization has been suggsted to occur under normal[Ca2+]c in intact cells (Okazaki and Tazawa 1986a, b), its absencesuggests that some cytoplasmic factors, which induce the membranedepolarization in a Ca2+-independent manner, are lost in tonoplast-removedcells.
1 Present address: Department of Biology, Osaka Medical College,Sawaragi-cho 2-41, Takatsuki, Osaka 569, Japan. (Received October 22, 1986; Accepted March 31, 1987) 相似文献
9.
Nakamura Yoshiyuki; Kasamo Kunihiro; Sakata Makato; Ohta Eiji 《Plant & cell physiology》1992,33(2):139-149
Extrusion of protons as a response to high-NaCl stress in intactmung bean roots was investigated at different external concentrationsof Ca2+ ions ([Ca2+]ex). The extrusion of protons was graduallyenhanced in the roots exposed to 100 mM NaCl, and high [Ca2+]exdiminished this enhancement of the extrusion. Vesicles of plasmalemmaand tonoplast were prepared from the roots and the H+-translocatingATPase (H+-ATPase) activities associated with the two typesof membrane and the H+-pyrophosphatase (H+-PPase) activity ofthe tonoplast were assayed. The plasmalemma ATPase was stimulatedin parallel with dramatic increases in the intracellular concentrationof Na+([Na+]in). High [Ca2+]ex prevented the increase in [Na+]inand diminished the stimulation of ATPase activity. The tonoplastATPase showed a rapid response to salt stress and was similarlystimulated even at high [Ca2+]M. The activities of both ATPaseswere, however, insensitive to concentrations of Na+ ions upto 100 HIM. By contrast, H+-PPase activity of the tonoplastwas severely inhibited with increasing [Na+]in under salt stressand recovered with high [Ca2+]ex. These findings suggest thathigh-NaCl stress increases the intracellular concentration ofNa+ ions in mung bean roots, which inhibits the tonoplast H+-PPase,and the activity of the plasmalemma H+-ATPase is thereby stimulatedand regulates the cytoplasmic pH. (Received March 26, 1991; Accepted December 13, 1991) 相似文献
10.
Temporal relationship between the action potential and the changein cytosolic Ca2+ concentration was investigated in cells offour species of Characeae, Chara corallina, Nitellopsis obtusa,Nitella flexilis and Nitella axilliformis. The Ca2+ transientwas detected by light emission from Ca2+-sensitive photoproteinaequorin injected into the cytoplasm. Action potential was triggeredby an outward or sometimes inward electric current pulse of2050 ms in most cases. In all species the action potentialstarted at almost the same time as the time at which the lightemission from aequorin began to increase. Also the peak of actionpotential almost coincided with that of light emission, whichis in contrast with the slower Ca2+ transient in Chara reportedby Thiel et al. [(1997) J. Exp. Bot. 48: 609]. A discussionwas made on the origin of Ca2+ transient and the ionic processesduring membrane excitation. (Received July 2, 1998; Accepted October 5, 1998) 相似文献
11.
Protoplasts and vacuoles were isolated from immature apple fruit(Malus pumila Mill. cv. Golden Delicious). ATP-stimulated Ca2+uptake was identified in both protoplast vesicles and tonoplastvesicles. The apparent Km for Ca2+ of the tonoplast transportsystem was 43.4 µM. The pH optima were 7.2 and 6.7 forCa2+ transport by protoplast and tonoplast vesicles, respectively.Ca2+ transport in tonoplast vesicles was strongly inhibitedby the calmodulin antagonists fluphenazine and N-(6-aminohexyl)-5-chloro-l-naphthalensulfonamidehydrochloride (W-7), while N-aminohexyl)-l-naphthalensulfonamidehydrochloride (W-5) was relatively ineffective. Addition ofexogenous calmodulin stimulated transport by 35%. Ca2+ uptakewas inhibited by vanadate, but not by the ionophores carbonylcyanidem-chlorophenyl hydrazone (CCCP) or valinomycin. The resultsindicate that apple tonoplasts have a Ca2+ transport systemthat is driven by the direct hydrolysis of ATP, and may be calmodulindependent.
1Present address: Morioka Branch, Fruit Tree Research Station,Ministry of Agriculture, Forestry and Fisheries, Shimokuriyagawa,Morioka 020-01, Japan. To whom reprint requests should be addressed. (Received October 18, 1985; Accepted January 29, 1986) 相似文献
12.
Internodal cells of Chara australis were subjected to two consecutiveintracellular perfusions with a Ca2+-free EGTA medium whichdisintegrated the tonoplast within about 10 minutes and thenwith a Ca2+-buffered medium. All perfusion media usually contained1 mM ATP. To stop the electrogenic pump, the internode was depletedof intracellular ATP. The excitability of the plasmalemma wasnot significantly influenced by intracellular free Ca2+ concentrationsup to 104 M. To trigger action potentials, minimum currentdensities of 1 to 2 µA cm2 had to be applied atall tested Ca2+ concentrations. In the absence of cytoplasmicATP, excitability was completely lost at all Ca2+ concentrations.
1 Present address: Botanisches Institut der Universit?t Bonn,Venusbergweg 22, D-5300 Bonn, FRG. (Received September 22, 1984; Accepted March 6, 1985) 相似文献
13.
A theoretical model of calcium signaling is presented that simulates oscillations of cytoplasmic calcium concentration ([Ca2+]cyt) in stomatal guard cells under the action of abscisic acid. The model is based on the kinetics of inositol 1,4,5-trisphosphate-sensitive calcium channels of endoplasmic reticulum and cyclic ADP-ribose-sensitive calcium channels of the tonoplast. The operation of two energy-dependent pumps—the Ca2+-ATPase of the endoplasmic reticulum and the Ca2+/H+ antiporter of the tonoplast—is also included in the model. It is shown that the removal of excessive Ca2+ from the cytoplasm by the tonoplast Ca2+/H+ antiporter is the main factor accounting for generation of [Ca2+]cyt oscillations at a wide range of ABA concentrations (0.01–1 M). The long period of [Ca2+]cyt oscillations in plant cells is explained by a slow release from inhibition of inositol 1,4,5-trisphosphate-gated calcium channels. 相似文献
14.
Nakamura Yoshiyuki; Ogawa Tomoko; Kasamo Kunihiro; Sakata Makoto; Ohta Eiji 《Plant & cell physiology》1992,33(7):849-858
The cytoplasmic pH and the vacuolar pH in root-tip cells ofintact mung bean seedlings under high-NaCl stress were measuredby in vivo 31P-nuclear magnetic resonance (31P-NMR) spectroscopy.When roots were incubated with high levels (100 mM) of NaClat the control external concentration (0.5 mM) of Ca2+ ions,the vacuolar pH increased rapidly from 5.6 to 6.2 within 3 h,while the cytoplasmic pH only decreased by a mere 0.1 pH uniteven after a 24-h incubation under high-NaCl conditions. Theincrease in vacuolar pH induced by the high-NaCl stress wasdiminished by an increase in the external concentration of Ca2+ions from 0.5 mM to 5 mM. The intracellular concentration ofNa+ ions in the root-tip cells increased dramatically upon perfusionof the root cells with 100 mM NaCl, and high external levelsof Ca2+ ions also suppressed the in flow of Na+ ions into thecells. The vacuolar alkalization observed in salt-stressed rootsmay be related to the inhibition of an H+-translocating pyrophosphatasein the tonoplast, caused by the increase in the cytoplasmicconcentration of Na+ ions. It is suggested that, although thevacuolar pH increased markedly under salt stress, the cytoplasmicpH was tightly regulated by some unidentified mechanisms, suchas stimulation of the H+-translocating ATPase of the plasmalemma,in roots of mung bean under salt stress. (Received April 18, 1992; Accepted July 6, 1992) 相似文献
15.
Summary The mechanism of the cessation of cytoplasmic streaming upon membrane excitation inCharaceae internodal cells was investigated.Cell fragments containing only cytoplasm were prepared by collecting the endoplasm at one cell end by centrifugation. In such cell fragments lacking the tonoplast, an action potential induced streaming cessation, indicating that an action potential at the plasmalemma alone is enough to stop the streaming.The active rotation of chloroplasts passively flowing together with the endoplasm also stopped simultaneously with the streaming cessation upon excitation. The time lag or interval between the rotation cessation and the electrical stimulation for inducing the action potential increased with the distance of the chloroplasts from the cortex. The time lag was about 1 second/15 m, suggesting that an agent causing the rotation cessation is diffused throughout the endoplasm.Using internodes whose tonoplast was removed by replacing the cell sap with EGTA-containing solution (tonoplast-free cells,Tazawa
et al. 1976), we investigated the streaming rate with respect to the internal Ca2+ concentration. The rate was roughly identical to that of normal cells at a Ca2+ concentration of less than 10–7 M. It decreased with an increase in the internal Ca2+ concentration and was zero at 1 mM Ca2+.The above results, together with the two facts that Ca2+ reversibly inhibits chloroplast rotation (Hayama andTazawa, unpublished) and the streaming in tonoplast-free cells does not stop upon excitation (Tazawa
et al. 1976), lead us to conclude that a transient increase in the Ca2+ concentration in the cytoplasm directly stops the cytoplasmic streaming. Both Ca influxes across the resting and active membranes were roughly proportional to the external Ca2+ concentration, which did not affect the rate of streaming recovery. Based on these results, several possibilities for the increase in Ca2+ concentration in the cytoplasm causing streaming cessation were discussed. 相似文献
16.
Kuba M Higure Y Susaki H Hayato R Kuba K 《American journal of physiology. Cell physiology》2007,292(2):C896-C908
How the endoplasmic reticulum (ER) and mitochondria communicate with each other and how they regulate plasmalemmal Ca2+ entry were studied in cultured rat brown adipocytes. Cytoplasmic Ca2+ or Mg2+ and mitochondrial membrane potential were measured by fluorometry. The sustained component of rises in cytoplasmic Ca2+ concentration ([Ca2+]i) produced by thapsigargin was abolished by removing extracellular Ca2+, depressed by depleting extracellular Na+, and enhanced by raising extracellular pH. FCCP, dinitrophenol, and rotenone caused bi- or triphasic rises in [Ca2+]i, in which the first phase was accompanied by mitochondrial depolarization. The FCCP-induced first phase was partially inhibited by oligomycin but not by ruthenium red, cyclosporine A, U-73122, a Ca2+-free EGTA solution, and an Na+-free solution. The FCCP-induced second phase paralleling mitochondrial repolarization was partially blocked by removing extracellular Ca2+ and fully blocked by oligomycin but not by thapsigargin or an Na+-deficient solution, was accompanied by a rise in cytoplasmic Mg2+ concentration, and was summated with a high pH-induced rise in [Ca2+]i, whereas the extracellular Ca2+-independent component was blocked by U-73122 and cyclopiazonic acid. The FCCP-induced third phase was blocked by removing Ca2+ but not by thapsigargin, depressed by decreasing Na+, and enhanced by raising pH. Cyclopiazonic acid-evoked rises in [Ca2+]i in a Ca2+-free solution were depressed after FCCP actions. Thus mitochondrial uncoupling causes Ca2+ release, activating Ca2+ release from the ER and store-operated Ca2+ entry, and directly elicits a novel plasmalemmal Ca2+ entry, whereas Ca2+ release from the ER activates Ca2+ accumulation in, or release from, mitochondria, indicating bidirectional mitochondria-ER couplings in rat brown adipocytes. plasmalemmal calcium entry; calcium release; mitochondrial depolarization; FCCP 相似文献
17.
An internode of Chara was permeabilized as described by Shimmenand Tazawa [(1983) Protoplasma 117:93]. The Cl effluxof the permeabilized cell increased when the extracellular Ca2+concentration was increased, and the degree of the increasewas dependent on the Ca2+ concentration. This suggests thatthe Cl channel in the tonoplast was activated by Ca2+. (Received May 22, 1987; Accepted October 21, 1987) 相似文献
18.
Effects of cytoplasmic Ca2+ on the electrical properties ofthe plasma membrane were investigated in tonoplast-free cellsof Chara australis that had been internally perfused with media,containing either 1 mM ATP to fuel the electrogenic pump orhexokinase and glucose to deplete the ATP and stop the pump. In the presence of ATP, cytoplasmic Ca2+ up to 2.5?105M did not affect the membrane potential (about -190 mV), butmembrane resistance decreased uniformly with increasing [Ca2+]i.In the absence of ATP, the membrane potential, which was onlyabout -110 mV, was depolarized further by raising [Ca2+]i from1.4?106 to 2.5?105 M. Membrane resistance, whichwas nearly the twofold that of ATP-provided cells, decreasedmarkedly with an increase in [Ca2+]i from zero to 1.38?106M, but showed no change for further increases. Internodal cellsof Nitellopsis obtusa were more sensitive to intracellular Ca2+with respect to membrane potential than were those of Charaaustralis, reconfirming the results obtained by Mimura and Tazawa(1983). The effect of cytoplasmic Ca2+ on the ATP-dependent H+ effluxwas measured. No marked difference in H+ effluxes was detectedbetween zero and 2.5?105 M [Ca2+]i; but, at 104M the ATP-dependent H+ efflux was almost zero. Ca2+ efflux experimentswere done to investigate dependencies on [Ca2+]i and [ATP]i.The efflux was about 1 pmol cm2 s1 at all [Ca2+]iconcentrations tested (1.38?106, 2.5?105, 104M).This value is much higher than the influx reported by Hayamaet al. (1979), and this efflux was independent of [ATP]i. Thepossibility of a Ca2+-extruding pump is discussed.
1 Present address: Botanisches Institut der Universit?t Bonn,Venusbergweg 22, 5300 Bonn, F.R.G. (Received September 22, 1984; Accepted February 19, 1985) 相似文献
19.
低温严重影响植物的生长, 低温刺激可引起植物细胞中Ca2+浓度迅速升高。以拟南芥(Arabidopsis thaliana) CBF1 超表达突变体为材料, 研究了低温处理时CBF1基因的表达情况及胞质Ca2+的浓度变化。结果表明, CBF1本身可受低温诱导。同时将水母发光蛋白基因转入该拟南芥突变体中并检测Ca2+的浓度变化, 发现低温刺激时突变体细胞质中Ca2+的浓度变化幅度明显高于野生型, 但液泡的胞质面两侧Ca2+的浓度变化相似。用EGTA和LaCl3处理拟南芥后, 胞质Ca2+的浓度升高被抑制, 并且CBF1突变体及对照胞质中的Ca2+浓度下降到同一水平。上述结果表明, Ca2+参与了CBF1应答低温信号的转导过程, 并且CBF1超表达突变体可能是通过提高胞质Ca2+浓度来提高植物的抗低温胁迫能力。 相似文献
20.
The effects of modification of extracellular concentrationsof Ca2+ and C on mechano-perception were studied in internodalcells of Chara corallina. Cells were stimulated by droppinga piece of glass tubing on them, and the resulting receptorpotentials and action potentials were analyzed. When the Ca2+concentration was extremely lowered by adding EGTA, the amplitudesof both receptor potentials and action potentials were attenuated,suggesting the involvement of Ca2+ channels. However, the possibilityremained that attenuation of the amplitude of the receptor potentialwas caused by modification of membrane characteristics by extremelowering of [Ca2+]o. When the plasma membrane was depolarizedto about 0 mV by adding 100 mM KC1, responses in the negativedirection were induced upon mechanical stimulation. When theplasma membrane was depolarized by adding 50 mM K2SO4, responsesin the positive direction were induced. Thus, Cl channelsmay be involved in responses induced by mechanical stimulationunder K+-induced depolarization. (Received January 16, 1996; Accepted March 25, 1997) 相似文献