Hyperpolarization-activated inward chloride current in protoplasts from suspension-cultured carrot cells

Summary Plasmalemmal ionic currents from enzymatically-isolated protoplasts of suspension-cultured carrot cells were investigated by patch-clamp techniques. Among other currents, a novel hyperpolarization-activated, inwardly-rectifying, whole-cell current was observed. The activation of this current was fast in onset, and for large hyperpolarizations a characteristic, rapid voltage-dependent inactivation was seen. Ion substitution experiments indicate that this inward current was due mainly to efflux of chloride ions. No dependence on either internal or external calcium was found, and internal MgATP was not necessary. Surprisingly, zinc did not block this current. In hyperpolarized outside-out patches, inward single-channel chloride currents having an elementary conductance of ca. 100 pS were observed. The open probability increased with hyperpolarization. Similar single-channel currents were activated by slight negative pressure applied to the pipette. These chloride currents could contribute both to the control of membrane potential and in the regulation of osmotic balance in carrot cells.Abbreviations BAPTA 1,2-bis (2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid - 2,4-D 2,4-dichlorophenoxyacetic acid - E_x Nernst equilibrium potential for ion x - NMDG N-methyl-D-glucamine - PMSF phenylmethylsulfonyl fluoride     

Increases of T-type Ca2+ current in heart cells of the cardiomyopathic hamster

In the present study, the whole-cell voltage clamp technique was used in order to record the T- and L-type Ca²⁺ currents in single heart cells of newborn and young normal and hereditary cardiomyopathic hamsters. Our results showed that the I/V relationship curve as well as the kinetics of the L-type Ca²⁺ currents (I_Ca(L)) in both normal and cardiomyopathic heart cells were the same. However, the proportion of myocytes from normal heart hamster that showed L-type I_Ca was less than that of heart cells from cardiomyopathic hamster. The I/V relationship curve of the T-type I_Ca (I_Ca(T)) was the same in myocytes of both normal and cardiomyopathic hamsters. The main differences between I_Ca(T) of cardiomyopathic and normal hamster are a larger window current and the proportion of ventricular myocytes that showed this type of current in cardiomyopathic hamster. The high density of I_Ca(T) as well as the large window current and proportion of myocytes showing I_Ca(T) may explain in part Ca²⁺ overload observed in cardiomyopathic heart cells of the hamster.     

Excitability of Paramecium and the significance of negative surface charges

Summary On the basis of a model presented in a previous paper (Hook and Hildebrand, 1979) the influence of external cation concentrations [K⁺]₀, [Ca²⁺]₀ and of membrane voltage V_m (i.e. the actual potential difference between the two membrane faces) on the locomotor behavior of Paramecium is theoretically analyzed. In an extended model system we discuss the negative feedback of intraciliary calcium [Ca²⁺]_i on the excitability of the ciliary membrane. While a fast blocking of Ca channels is mediated by increased [Ca²⁺]_i and accounts for the short duration of action potentials, a slow [Ca²⁺ ]_i-dependent denaturation of channel molecules is assumed to determine excitability changes of Paramecium on a long time scale.It is emphasized that the duration of long-lasting ciliary reversal which reflects the excitability is not a direct function of the cation ratio J_u [K⁺]₀/[Ca²⁺] ₀ ^1/2 but rather of the membrane potential V_m.Introduction of negative surface charges can well explain why for a series of different [K⁺]₀, [Ca²⁺]₀ but constant J_a value the excitability is unchanged despite corresponding shifts in measured membrane potentials.     

Inhibition of Mg2+ current by single-gene mutation in Paramecium

Eccentric is a newly-isolated mutant of Paramecium tetraurelia that fails to swim backwards in response to Mg²⁺. In the wild type, this backward swimming results from Mg²⁺ influx via a Mg²⁺-specific ion conductance (I _Mg. Voltage-clamp analysis confirmed that, as suspected, step changes in membrane potential over a physiological range fail to elicit I _Mg from eccentric. Further electrophysiological investigation revealed a number of additional ion-current defects in eccentric: (i) The Ca²⁺ current activated upon depolarization inactivates more slowly in eccentric than in the wild type, and it requires longer to recover from this inactivation. (ii) The Ca²⁺-dependent Na⁺ current deactivates significantly faster in the mutant, (iii) The two K⁺ currents observed upon hyperpolarization are reduced by >60% in eccentric. It is difficult to envision how these varied pleiotropic effects could result from loss of a single ion current. Rather, they suggest that the eccentric mutation affects a global regulatory system. Two plausible hypotheses are discussed.We are grateful to Dr. Yoshiro Saimi for his comments and suggestions on this work, and for the support of the Lucille P. Markey Charitable trust and the National Institutes of Health (GM22714 and GM38646).     

Ca2+ transport and chemoreception in Paramecium

Intracellular Ca²⁺ levels in Paramecium must be tightly controlled, yet little is understood about the mechanisms of control. We describe here indirect evidence that a phosphoenzyme intermediate is the calmodulin-regulated plasma membrane Ca²⁺ pump and that a Ca²⁺-ATPase activity in pellicles (the complex of cell body surface membranes) is the enzyme correlate of the plasma membrane pump protein. A change in Ca²⁺ pump activity has been implicated in the chemoresponse of paramecia to some attractant stimuli. Indirect support for this is demonstrated using mutants with different modifications of calmodulin to correlate defects in chemoresponse with altered Ca²⁺ homeostasis and pump activity.Abbreviations EGTA ethyleneglycol tetra-acetate - ER endoplasmic reticulum - IBMX isobutyl methylxanthine - I _che index of chemokinesis - Mops 3-[N-morpholino] propanesulfonic acid - PEI phosphoenzyme intermediate - STEN sucrose, TRIS, EDTA, sodium chloride - TCA trichloroacetic acid - TRIS tris[hydroxymethyl] aminomethane     

In vivo activation of cirral movement in Stylonychia by calcium

Summary Motor responses of cirri (= organelles consisting of bundles of cilia) in the protozoan Stylonychia are elicited by positive or negative shifts of the membrane voltage from its resting state. The same responses are evoked at voltages near the Ca²⁺ equilibrium potential (E_Ca) applying extremely positive steps under voltage clamp. Motor responses recorded at large positive voltages approaching E_Ca from the negative side corresponded to cirral activation following physiological depolarization from the resting potential (DCA). The hyperpolarization-induced activation of the cirri (HCA) was documented during step potentials positive to E_Ca, suggesting that the observed HCA of the cirri resulted from an efflux of Ca²⁺ from the ciliary space as compared with DCA, which is related to Ca²⁺ influx. The ciliary responses were graded functions of the rising outward or inward driving force for Ca²⁺. Slopes of reciprocal plots of response latencies near E_Ca as a function of membrane potential indicate a removal of Ca²⁺ during HCA which exceeds the free intraciliary Ca²⁺ content at rest. It is suggested that this excess Ca²⁺ is released from axonemal binding sites.     

Neurohormone D induces ionic current changes in cockroach central neurones

The octapeptide neurohormone D (NHD), a member of the family of adipokinetic hormones (AKH-peptides), increases the frequency of spontaneous activity in dorsal unpaired median (DUM) neurones isolated from the terminal ganglion of the cockroach Periplaneta americana. The increase in spike frequency is accompanied by changes in the shape and the amplitude of the single action potentials, e.g. a more pronounced afterhyperpolarization. Effects of NHD on membrane currents were investigated in these DUM cells with whole-cell voltage-clamp measurements. A voltage-independent Ca²⁺ current flowing at the resting potential (I_Ca,R) was found. NHD, at nanomolar concentrations, enhanced this I_Ca,R in a concentration-dependent manner. 0.1 mM Cd²⁺markedly reduced I_Ca,R and in this case I_Ca,R was hardly potentiated by NHD.In the presence of NHD a fast activating Ca²⁺-dependent K⁺current sensitive to charybdotoxin and to low concentrations of tetraethylammonium was augmented. The enhanced afterhyperpolarization of action potentials can be accounted for by the increase in the Ca²⁺-dependent K⁺ current.The changes of the membrane currents induced by NHD are discussed with respect to further effects on the spike pattern and in relation to the previously described mode of action of AKH-peptides in other preparations.Abbreviations NHD neurohormone D - AKH adipokinetic hormone     

Sub-second calcium coupling between outside medium and subplasmalemmal stores during overstimulation/depolarisation-induced ciliary beat reversal in Paramecium cells

As amply documented by electrophysiology, depolarisation in Paramecium induces a Ca(2+) influx selectively via ciliary voltage-dependent Ca(2+)-channels, thus inducing ciliary beat reversal. Subsequent downregulation of ciliary Ca(2+) has remained enigmatic. We now analysed this aspect, eventually under overstimulation conditions, by quenched-flow/cryofixation, combined with electron microscope X-ray microanalysis which registers total calcium concentrations, [Ca]. This allows to follow Ca-signals within a time period (> or =30ms) smaller than one ciliary beat ( approximately 50ms) and beyond. Particularly under overstimulation conditions ( approximately 10(-5)M Ca(2+) before, 0.5mM Ca(2+) during stimulation) we find in cilia a [Ca] peak at approximately 80ms and its decay to near-basal levels within 110ms (90%) to 170ms (100% decay). This [Ca] wave is followed, with little delay, by a [Ca] wave into subplasmalemmal Ca-stores (alveolar sacs), culminating at approximately 100ms, with a decay to original levels within 170ms. Also with little delay [Ca] slightly increases in the cytoplasm below. This implies rapid dissipation of Ca(2+) through the ciliary basis, paralleled by a rapid, transient uptake by, and release from cortical stores, suggesting fast exchange mechanisms to be analysed as yet. This novel type of coupling may be relevant for some phenomena described for other cells.     

Selective modulation of L-type calcium current by magnesium lithospermate B in guinea-pig ventricular myocytes

Magnesium lithospermate B (MLB) is the main water-soluble principle of Salviae Miltiorrhizae Radix (also called as 'Danshen' in the traditional Chinese medicine) for the treatment of cardiovascular diseases. MLB was found to possess a variety of pharmacological actions. However, it is unclear whether and how MLB affects the cardiac ion channels. In the present study, the effects of MLB on the voltage-activated ionic currents were investigated in single ventricular myocytes of adult guinea pigs. MLB reversibly inhibited L-type Ca(2+) current (I(Ca,L)). The inhibition was use-dependent and voltage-dependent (the IC(50) value of MLB was 30 microM and 393 microM, respectively, at the holding potential of -50 mV and -100 mV). In the presence of 100 microM MLB, both the activation and steady-state inactivation curves of I(Ca,L) were markedly shifted to hyperpolarizing membrane potentials, whereas the time course of recovery of I(Ca,L) from inactivation was not altered. MLB up to 300 microM had no significant effect on the fast-inactivating Na(+) current (I(Na)), delayed rectifier K(+) current (I(K)) and inward rectifier K(+) current (I(K1)). The results suggest that the voltage-dependent Ca(2+) antagonistic effect of MLB work in concert with its antioxidant action for attenuating heart ischemic injury.     

Calcium current kinetics in young and aged human cultured myotubes

There is evidence that the complex process of sarcopenia in human aged skeletal muscle is linked to the modification of mechanisms controlling Ca²⁺ homeostasis. To further clarify this issue, we assessed the changes in the kinetics of activation and inactivation of T- and L-type Ca²⁺ currents in in vitro differentiated human myotubes, derived from satellite cells of healthy donors aged 2, 12, 76 and 86 years. The results showed an age-related decrease in the occurrence of T- and L-type currents. Moreover, significant age-dependent alterations were found in L-(but not T) type current density, and activation and inactivation kinetics, although an interesting alteration in the kinetics of T-current inactivation was observed. The T- and L-type Ca²⁺ currents play a crucial role in regulating Ca²⁺ entry during satellite cells differentiation and fusion into myotubes. Also, the L-type Ca²⁺ channels underlie the skeletal muscle excitation–contraction coupling mechanism. Thus, our results support the hypothesis that the aging process could negatively affect the Ca²⁺ homeostasis of these cells, by altering Ca²⁺ entry through T- and L-type Ca²⁺ channels, thereby putting a strain on the ability of human satellite cells to regenerate skeletal muscle in elderly people.     

Centrin is essential for the activity of the ciliary reversal-coupled voltage-gated Ca2+ channels

Voltage-gated Ca(2+) channels play a critical role in controlling Ca(2+) entry in various cells. Ciliary reversal in Paramecium depends on the Ca(2+) influx through voltage-gated Ca(2+) channels on the ciliary membrane. One of the voltage-gated Ca(2+) channel mutants in Paramecium caudatum, cnrC, neither produces Ca(2+) action potentials nor responds to any depolarizing stimuli. Here, we report that the cnrC(+) gene product is P. caudatum centrin (Pccentrin1p), a member of the Ca(2+)-binding EF-hand protein superfamily. The Pccentrin1p gene of cnrC was found to contain a single-base deletion, a mutation that caused the loss of the fourth EF-hand of Pccentrin1p. Moreover, the wild-type Ca(2+) channel function was impaired by Pccentrin1p gene silencing, leading to the loss of current-evoked Ca(2+) action potentials and stimulated ciliary reversal. These results demonstrate that Pccentrin1p is indispensable for the activity of the voltage-gated Ca(2+) channels that control ciliary reversal in Paramecium.     

An increase in intracellular Ca2+ is involved in pronephric tubule differentiation in the amphibian Xenopus laevis

The pronephros is the first kidney to develop and is the functional embryonic kidney in lower vertebrates. It has previously been shown that pronephric tubules can be induced to form ex vivo in ectodermal tissue by treatment with activin A and retinoic acid. In this study, we investigated the role of Ca(2+) signaling in the formation of the pronephric tubules both in intact Xenopus embryos and ex vivo. In the ex vivo system, retinoic acid but not activin A stimulated the generation of Ca(2+) transients during tubule formation. Furthermore, tubule differentiation could be induced by agents that increase the concentration of intracellular Ca(2+) in activin A-treated ectoderm. In addition, tubule formation was inhibited by loading the ectodermal tissue with the Ca(2+) chelator, BAPTA-AM prior to activin A/retinoic acid treatment. In intact embryos, Ca(2+) transients were also recorded during tubule formation, and photo-activation of the caged Ca(2+) chelator, diazo-2, localized to the pronephric domain, produced embryos with a shortened and widened tubule phenotype. In addition, the location of the Ca(2+) transients observed, correlated with the expression pattern of the specific pronephric tubule gene, XSMP-30. These data indicate that Ca(2+) might be a necessary signal in the process of tubulogenesis both ex vivo and in intact embryos.     

Effects of extremely low frequency electromagnetic fields on intracellular calcium transients in cardiomyocytes

Abstract

Calcium transients play an essential role in cardiomyocytes and electromagnetic fields (EMF) and affect intracellular calcium levels in many types of cells. Effects of EMF on intracellular calcium transients in cardiomyocytes are not well studied. The aim of this study was to assess whether extremely low frequency electromagnetic fields (ELF-EMF) could affect intracellular calcium transients in cardiomyocytes. Cardiomyocytes isolated from neonatal Sprague-Dawley rats were exposed to rectangular-wave pulsed ELF-EMF at four different frequencies (15?Hz, 50?Hz, 75?Hz and 100?Hz) and at a flux density of 2?mT. Intracellular calcium concentration ([Ca²⁺]_i) was measured using Fura-2/AM and spectrofluorometry. Perfusion of cardiomyocytes with a high concentration of caffeine (10?mM) was carried out to verify the function of the cardiac Na⁺/Ca²⁺ exchanger (NCX) and the activity of sarco(endo)-plasmic reticulum Ca²⁺-ATPase (SERCA2a). The results showed that ELF-EMF enhanced the activities of NCX and SERCA2a, increased [Ca²⁺]_i baseline level and frequency of calcium transients in cardiomyocytes and decreased the amplitude of calcium transients and calcium level in sarcoplasmic reticulum. These results indicated that ELF-EMF can regulate calcium-associated activities in cardiomyocytes.     

In rat hepatocytes, different adenosine receptor subtypes use different secondary messengers to increase the rate of ureagenesis

In rat hepatocytes, the role of cAMP and Ca(2+) as secondary messengers in the ureagenic response to stimulation of specific adenosine receptor subtypes was explored. Analyzed receptor subtypes were: A(1), A(2A), A(2B) and A(3). Each receptor subtype was stimulated with a specific agonist while blocking all other receptor subtypes with a battery of specific antagonists. For the A(1) and A(3) adenosine receptor subtypes, the secondary messenger was the cytoplasmic Ca(2+) concentration ([Ca(2+)](cyt)). Accordingly, the A(1) or A(3)-mediated increase in [Ca(2+)](cyt) and in ureagenic activity were both inhibited by chelating Ca(2+) with either EGTA or BAPTA-AM. Also, Gd(3+) blocked both the increase in [Ca(2+)](cyt) and ureagenesis, suggesting that a Ca(2+) channel may be involved in the response to both A(1) and A(3). A partial effect was observed with the sarcoplasmic reticulum Ca(2+)-ATPase inhibitor thapsigargin. The concentration of cyclic AMP ([cAMP]) increased in response to stimulation of either the A(2A) or the A(2B) adenosine receptor subtypes, while it decreased slightly in response to stimulation of either A(1) or A(3). The stimulation of either the A(2A) or A(2B) adenosine receptor subtypes resulted in an increase in [cAMP] and an ureagenic response which were not sensitive to EGTA, BAPTA-AM, Gd(3+) or to thapsigargin. In addition, the adenylyl cyclase inhibitor MDL12,330A blocked the ureagenic response to A(2A) and A(2B), but not the response to either A(1) or A(3). Our results indicate that in the ureagenic liver response to adenosine, the secondary messenger for both, the A(1) and A(3) adenosine receptor subtypes is [Ca(2+)](cyt), while the message from the A(2A) and A(2B) adenosine receptor subtypes is relayed by [cAMP].     

Methamphetamine directly accelerates beating rate in cardiomyocytes by increasing Ca entry via L-type Ca channel

Methamphetamine induces several cardiac dysfunctions, which leads to arrhythmia, cardiac failure and sudden cardiac death. Although these cardiac alterations elicited by methamphetamine were thought to be due to an indirect action of methamphetamine, namely, an excessive catecholamine release from synaptic terminals, while it seems likely that methamphetamine directly modulates the functioning of cardiomyocytes independent of neurotransmitters. However, the direct effects of methamphetamine on cardiomyocytes are still not clear. We show that methamphetamine directly accelerates the beating rate and alters Ca²⁺ oscillation pattern in cultured neonatal rat cardiomyocytes. Adrenergic receptor antagonists did not block the methamphetamine-induced alterations in cardiomyocytes. Treatment with a ryanodine receptor type 2 inhibitor and a sarcoplasmic reticulum Ca²⁺-ATPase inhibitor did not affect these responses, either. In contrast, the L-type Ca²⁺ channel inhibitor nifedipine eradicated these responses. Furthermore, methamphetamine elevated the internal free Ca²⁺ concentration in HEK-293T cells stably transfected with the L-type Ca²⁺ channel α1C subunit. In neonatal rat cardiomyocytes, methamphetamine accelerates beating rate and alters Ca²⁺ oscillation pattern by increasing Ca²⁺ entry via the L-type Ca²⁺ channels independent of any neurotransmitters.     

Possible mechanism of ciliary stimulation by extracellular ATP: Involvement of calcium-dependent potassium channels and exogenous Ca2+

Summary Ciliary motility was examined optically in tissue cultures from frog palate epithelium and frog's esophagus as a function of extracellular concentration of adenosine 5-triphosphate (ATP) and related compounds. The addition of micromolar concentration of ATP caused a strong enhancement of frequency and wave velocity in the direction of the effective stroke. Since adenosine 5-[, imido]-triphosphate (AMP-PNP), a nonhydrolyzable analog of ATP, produces the same effects, ATP hydrolysis is not required. The overall potency is ATP AMP-PNP>ADP adenosine>AMP. It is suggested that both the phosphate and the base moieties are involved in ATP binding.The enhancement of ciliary activity by extracellular ATP is dependent on the presence of extracellular Ca²⁺, which can be replaced by extracellular Mg²⁺. The effect of a number of potent inhibitors of the voltage-gated calcium channels on the stimulation of ciliary activity by ATP were examined. No effect was detected in the concentration range within which these agents are specific. On the other hand, quinidine, a potent inhibitor of K⁺ (calcium-dependent) channels, inhibits the effect of ATP.The following model is suggested: exogenous ATP interacts with a membrane receptor in the presence of Ca²⁺, a cascade of events occurs which mobilizes intracellular calcium, thereby increasing the cytosolic free Ca²⁺ concentration which consequently opens the calcium-activated K⁺ channels, which then leads to a change in membrane potential. The ciliary response to these changes is the enhancement of ciliary activity.This work was supported by a grant from the Fund for Basic Research administered by the Israel Academy of Science and Humanities.     

Overexpression of SERCA2 ATPaase in vascular smooth muscle cells treated with oxidized low density lipoprotein

Oxidized low density lipoprotein (oxLDL) has been identified as a potentially important atherogenic factor. Atherosclerosis is characterized by the accumulation of lipid and calcium in the vascular wall. OxLDL plays a significant role in altering calcium homeostasis within different cell types. In our previous study, chronic treatment of vascular smooth muscle cells (VSMC) with oxLDL depressed Ca²⁺ _i homeostasis and altered two Ca²⁺ release mechanisms in these cells (IP₃ and ryanodine sensitive channels). The purpose of the present study was to further define the effects of chronic treatment with oxLDL on the smooth muscle sarcoplasmic reticulum (SR) Ca²⁺ pump. One of the primary Ca²⁺ uptake mechanisms in VSMC is through the SERCA2 ATPase calcium pump in the sarcoplasmic reticulum. VSMC were chronically treated with 0.005-0.1 mg/ml oxLDL for up to 6 days in culture. Cells treated with oxLDL showed a significant increase in the total SERCA2 ATPase content. These changes were observed on both Western blot and immunocytochemical analysis. This increase in SERCA2 ATPase is in striking contrast to a significant decrease in the density of IP₃ and ryanodine receptors in VSMC as the result of chronic treatment with oxLDL. This response may suggest a specific adaptive mechanism that the pump undergoes to attempt to maintain Ca²⁺ homeostasis in VSMC chronically exposed to atherogenic oxLDL.     

Effect of olvanil (N-vanillyl-cis-9-octadecenoamide) on cytosolic Ca2+ increase in renal tubular cells

In canine renal tubular cells, effect of olvanil, a presumed cannabinoid and vanilloid receptor modulator, on intracellular Ca2+ concentration ([Ca2+]i) was measured by using fura-2. Olvanil (5-100 microM) caused a rapid and sustained [Ca2+]i rise in a concentration-dependent manner. Olvanil-induced [Ca2+]i rise was prevented by 70 and 90% by removal of extracellular Ca2+ and La3+, respectively, but was not changed by dihydropyridines, verapamil and diltiazem. In Ca2+-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+-ATPase, caused a monophasic [Ca2+]i rise, after which the increasing effect of olvanil on [Ca2+]i was abolished; also, pretreatment with olvanil partly reduced thapsigargin-induced [Ca2+]i rise. U73122, an inhibitor of phoispholipase C, abrogated ATP-, but partly inhibited olvanil-, induced [Ca2+]i rise. Two cannabinoid receptor antagonists (AM251 and AM281; 5 microM) and a vanilloid receptor antagonist (capsazepine; 100 microM) did not alter olvanil (50 microM)-induced [Ca2+]i rise. These results suggest that olvanil rapidly increases [Ca2+]i in renal tubular cells, by stimulating both extracellular Ca2+ influx and intracellular Ca2+ release via mechanism(s) independent of stimulation of cannabinoid and vanilloid receptors.     

Noise of secretagogue-induced inward currents dependent on extracellular calcium in rat mast cells

We analyzed the noise of the inward currents induced by stimulation of rat peritoneal mast cells with compound 48/80 (48/80), a secretagogue, and examined the role of extracellular Ca2+ in generation of the large noise. In the presence of 2 mM Ca2+ in the external solution, the power density spectra of the 48/80-induced inward currents in most cells were fitted with the sum of two Lorentzian functions. The cut-off frequencies (fc) at -50 mV for the low and high frequency components were 16.3 +/- 7.3 (n = 10) and 180 +/- 95 (n = 9) Hz. Involvement of a cation-selective channel in the large noise was identified in some cells, but the single channel current amplitude estimated from parameters of the noise varied among cells (0.20-2.47 pA at -50 mV), thereby indicating that the currents were mediated by more than two classes of channel. The low frequency component of the 48/80-induced currents was suppressed by lowering the extracellular Ca2+ concentration to 1 microM with the addition of EGTA, without appreciable changes in the high frequency component. When the extracellular Ca2+ was reduced to 1 microM by EGTA 1 min prior to stimulation, 48/80 induced little or no currents in most cells and small currents in some cells. The power density spectra of the small currents were fitted mainly by a single Lorentzian curve with an fc of 150 +/- 5.8 Hz (n = 3). Re-admission of 1.3 mM Ca2+ produced a low frequency part of current noise with an fc of 18.8 (n = 2) Hz.(ABSTRACT TRUNCATED AT 250 WORDS)