Influence of the Membrane Potential on the Intracellular Light Induced Ca2+ -Concentration Change of the Limulus Ventral Photoreceptor Monitored by Arsenazo III under Voltage Clamp Conditions

1984 ◽  
Vol 39 (9-10) ◽  
pp. 986-992 ◽  
Author(s):  
I. Ivens ◽  
H. Stieve
Keyword(s):  
Voltage Clamp ◽  
Light Flash ◽  
Membrane Voltage ◽  
Ion Concentration ◽  
Arsenazo Iii ◽  
Substantial Part ◽  
Voltage Range ◽  
Intracellular Ca ◽  
Intracellular Calcium Ion ◽  
Pass Through

Abstract The light induced transmission change (Arsenazo signal) of an Arsenazo III injected ventral photoreceptor cell of Limulus polyphemus was studied under voltage clamp. The transmission change which represents a change of free intracellular calcium ion concentration, [Ca2+]i, was investigated for its dependence upon membrane voltage. The peak amplitude of the Arsenazo signal decreases in a linear fashion with the clamp voltage in the examined voltage range (from -80 to + 40 mV). In low Ca2+ saline ([Ca2+]e = 250 μᴍ) this decrease in the amplitude of the Arsenazo signal was more pronounced, while in saline with increased Ca2+ ([Ca2+]e = 40, 50 and 100 mᴍ), there is almost no change of the Arsenazo signal with varied membrane voltage. The recovery of the Arsenazo signal (i.e. recovery of the transmission back to the value before the light flash) is faster during hyperpolarization, this recovery being slowed down when the cell is depolarized. From these experiments it is concluded that a substantial part of the Arsenazo signal is due to a light induced influx of Ca2+ from the extracellular space across the cell membrane into the cytoplasma. Conceivably the Ca2+ could pass through light activated Na+ channels. Subsequently the increased intracellular Ca2+ is lowered to the preillumination level, by a membrane voltage dependent mechanism possibly an Na+-Ca2+ exchange. The data do not exclude the possibility that a part of the Ca2+ responsible for the Arsenazo signal is released from intracellular stores.

scholarly journals Neonatal Intermittent Hypoxia Leads to Long-Lasting Facilitation of Acute Hypoxia-Evoked Catecholamine Secretion From Rat Chromaffin Cells

2009 ◽  
Vol 101 (6) ◽  
pp. 2837-2846 ◽  
Author(s):  
Dangjai Souvannakitti ◽  
Ganesh K. Kumar ◽  
Aaron Fox ◽  
Nanduri R. Prabhakar
Keyword(s):  
Intermittent Hypoxia ◽  
Chromaffin Cells ◽  
Acute Hypoxia ◽  
Adult Life ◽  
Underlying Mechanism ◽  
Ion Concentration ◽  
Rat Pups ◽  
Intracellular Ca ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration

The objective of the present study was to examine the effects of intermittent hypoxia (IH) and sustained hypoxia (SH) on hypoxia-evoked catecholamine (CA) secretion from chromaffin cells in neonatal rats and assess the underlying mechanism(s). Experiments were performed on rat pups exposed to either IH (15-s hypoxia/5-min normoxia; 8 h/day) or SH (hypobaric hypoxia, 0.4 atm) or normoxia (controls) from P0 to P5. IH treatment facilitated hypoxia-evoked CA secretion and elevations in the intracellular calcium ion concentration ([Ca2+]i) and these responses were attenuated, but not abolished, by treatments designed to eliminate Ca2+ flux into cells (Ca2+-free medium or Cd2+), indicating that intracellular Ca2+ stores were augmented by IH. Norepinephrine (NE) and epinephrine (E) levels of adrenal medullae were elevated in IH-treated pups. IH treatment increased reactive oxygen species (ROS) production in adrenal medullae and antioxidant treatment prevented IH-induced facilitation of CA secretion, elevations in [Ca2+]i by hypoxia, and the up-regulation of NE and E. The effects of neonatal IH treatment on hypoxia-induced CA secretion and elevation in [Ca2+]i, CA, and ROS levels persisted in rats reared under normoxia for >30 days. In striking contrast, chromaffin cells from SH-treated animals exhibited attenuated hypoxia-evoked CA secretion. In SH-treated cells hypoxia-evoked elevations in [Ca2+]i, NE and E contents, and ROS levels were comparable with controls. These observations demonstrate that: 1) neonatal IH and SH evoke opposite effects on hypoxia-evoked CA secretion from chromaffin cells, 2) ROS signaling mediates the faciltatory effects of IH, and 3) the effects of neonatal IH on chromaffin cells persist into adult life.

scholarly journals Various non-digestible saccharides increase intracellular calcium ion concentration in rat small-intestinal enterocytes

2004 ◽  
Vol 92 (5) ◽  
pp. 751-755 ◽  
Author(s):  
Takuya Suzuki ◽  
Hiroshi Hara
Keyword(s):  
Capric Acid ◽  
Peak Level ◽  
Positive Control ◽  
Ion Concentration ◽  
Cellular Mechanisms ◽  
Before And After ◽  
Intracellular Ca ◽  
Intracellular Calcium Ion ◽  
Small Intestinal ◽  
Intestinal Enterocytes

We have previously shown that non-digestible saccharides (NDS) stimulate intestinal Ca absorption via tight junctions. However, the cellular mechanisms activated by the NDS are not yet known. We investigated the effects of four NDS, difructose anhydride (DFA) III, DFAIV, fructo-oligosaccharides, and maltitol, on intracellular Ca signalling in isolated rat small-intestinal enterocytes. The changes in intracellular Ca2+concentration were measured before and after the addition of capric acid (7·5 or 15 mmol/l, a positive control), glycerol, or each NDS (1 or 10 mmol/l) to fura-2-loaded enterocytes. Treatment with capric acid or each NDS caused an immediate and dose-dependent rise in intracellular Ca2+concentration. Mechanical and osmotic stimulation achieved by adding glycerol had no effect on intracellular Ca2+concentration. The intracellular Ca2+concentration in enterocytes treated with DFAIII and fructo-oligosaccharides reached a peak level at about 30 s after stimulation, but those treated with DFAIV and maltitol showed further increases after the initial rapid rise. The maximum change in intracellular Ca2+concentration obtained by the application of maltitol was higher than that of DFAIII at 10 mmol/l. These findings suggest that each of the four NDS directly stimulates rat enterocytes, and increases intracellular Ca2+concentration. Thus, molecular structure may be more important than the size of the NDS in the induction of Ca signalling in the cells.

Effects of membrane polarization on sarcoplasmic calcium release in skeletal muscle

1981 ◽  
Vol 213 (1190) ◽  
pp. 1-13 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Calcium Release ◽  
Calcium Transient ◽  
Ion Concentration ◽  
Arsenazo Iii ◽  
Muscle Fibres ◽  
Test Pulse ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration ◽  
Skeletal Muscle Fibres

Calcium release from the sarcoplasmic reticulum was investigated in voltage-clamped, tetrodotoxin-treated frog skeletal muscle fibres injected with arsenazo III. Short (5 ms) depolarizing pulses (test pulses) produced a transient change in arsenazo III absorption, signalling an increase in intracellular calcium ion concentration (calcium transient). Conditioning subthreshold depolarizations, which preceded the test pulse, potentiated the calcium transient triggered by the test pulse. Conditioning hyper-polarizations, applied either before or after the test pulse, inhibited the calcium transient. These effects of conditioning polarizations on the calcium transient may explain similar effects of subthreshold polarizations on muscle contraction that have previously been reported. The potentiating effect of subthreshold depolarizations was observed only when the test pulse was short (5 ms). The potentiating effect develops at -48 mV with a time constant of about 7 ms at 6.5°C; this seems to be slower than that predicted by the potential spread from the surface along the tubular system. Thus, part of the effect could arise from the coupling process between tubular depolarization and calcium release.

scholarly journals Glutamate Regulates IP3-Type and CICR Stores in the Avian Cochlear Nucleus

1999 ◽  
Vol 81 (4) ◽  
pp. 1587-1596 ◽  
Author(s):  
B. Maya Kato ◽  
Edwin W Rubel
Keyword(s):  
Phorbol Ester ◽  
Cochlear Nucleus ◽  
Metabotropic Glutamate Receptor ◽  
Ion Concentration ◽  
Metabotropic Glutamate ◽  
Highly Active ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration

Glutamate regulates IP3-type and CICR stores in the avian cochlear nucleus. Neurons of the avian cochlear nucleus, nucleus magnocellularis (NM), are activated by glutamate released from auditory nerve terminals. If this stimulation is removed, the intracellular calcium ion concentration ([Ca2+]i) of NM neurons rises and rapid atrophic changes ensue. We have been investigating mechanisms that regulate [Ca2+]i in these neurons based on the hypothesis that loss of Ca2+ homeostasis causes the cascade of cellular changes that results in neuronal atrophy and death. In the present study, video-enhanced fluorometry was used to monitor changes in [Ca2+]i stimulated by agents that mobilize Ca2+ from intracellular stores and to study the modulation of these responses by glutamate. Homobromoibotenic acid (HBI) was used to stimulate inositol trisphosphate (IP3)-sensitive stores, and caffeine was used to mobilize Ca2+ from Ca2+-induced Ca2+ release (CICR) stores. We provide data indicating that Ca2+responses attributable to IP3- and CICR-sensitive stores are inhibited by glutamate, acting via a metabotropic glutamate receptor (mGluR). We also show that activation of C-kinase by a phorbol ester will reduce HBI-stimulated calcium responses. Although the protein kinase A accumulator, Sp-cAMPs, did not have an effect on HBI-induced responses. CICR-stimulated responses were not consistently attenuated by either the phorbol ester or the Sp-cAMPs. We have previously shown that glutamate attenuates voltage-dependent changes in [Ca2+]i. Coupled with the present findings, this suggests that in these neurons mGluRs serve to limit fluctuations in intracellular Ca2+ rather than increase [Ca2+]i. This system may play a role in protecting highly active neurons from calcium toxicity resulting in apoptosis.

CaBPr facilitates intracellular diffusion for Ca pumping in distal convoluted tubule

1988 ◽  
Vol 255 (3) ◽  
pp. F558-F562 ◽  
Author(s):  
F. Bronner ◽  
W. D. Stein
Keyword(s):  
Vitamin D ◽  
Calcium Binding ◽  
Distal Convoluted Tubule ◽  
Ion Concentration ◽  
Electrochemical Gradient ◽  
Active Vitamin ◽  
Animal Data ◽  
Intracellular Diffusion ◽  
Intracellular Ca ◽  
Active Calcium

The system of renal Ca transport in the rat is modeled in terms of two classes of processes: a nonsaturable flux that predominates in the proximal tubule, and an active, vitamin D-dependent flux with major expression in the distal convoluted tubule. There transport is against an electrochemical gradient, with much of the efflux probably mediated by the Ca/Mg-ATPase. Calculations of the rate of free Ca diffusion in tubular cells indicate that an unaided flux would be only one-seventy-seventh of that found experimentally. It is suggested that the vitamin D-induced renal calcium binding protein, CaBPr, Mr approximately 28,000, in raising total cellular calcium by three orders of magnitude, increases the transcellular Ca flux and thus the free intracellular Ca ion concentration at the basolateral pole, allowing the Ca/Mg-ATPase to function near its maximum. Analysis of the rate of nonsaturable Ca flux throughout the kidney tubule suggests a paracellular pathway via bulk flow, following water that is driven osmotically. Evaluation of whole animal data in terms of these two classes of calcium fluxes indicates that our model is consistent with experimental observations and assigns a functional role to active calcium transport.

scholarly journals Intramural optical mapping of Vm and Cai2+ during long-duration ventricular fibrillation in canine hearts

2012 ◽  
Vol 302 (6) ◽  
pp. H1294-H1305 ◽  
Author(s):  
Wei Kong ◽  
Raymond E. Ideker ◽  
Vladimir G. Fast
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Short Duration ◽  
Action Potential Duration ◽  
Cycle Length ◽  
The Other ◽  
Membrane Voltage ◽  
Long Duration ◽  
Intracellular Ca ◽  
Rapid Pacing

Intramural gradients of intracellular Ca2+ (Cai2+) Cai2+ handling, Cai2+ oscillations, and Cai2+ transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Cai2+ handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Cai2+ handling contribute to LDVF, we measured membrane voltage ( Vm) and Cai2+ during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, Vm and Cai2+ progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed Vm upstrokes during pacing and LDVF. In conclusion, the fact that Vm upstrokes always preceded CaTs indicates that spontaneous Cai2+ oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong Vm-Cai2+ desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Cai2+ handling and may potentially contribute to LDVF maintenance.

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