Light- and voltage-dependent increases of calcium ion concentration in molluscan photoreceptors

1984 ◽  
Vol 51 (4) ◽  
pp. 745-752 ◽  
Author(s):  
J. Connor ◽  
D. L. Alkon

Changes in cytoplasmic calcium levels have been measured in photoreceptors from Hermissenda crassicornis using the indicator dye Arsenazo III. Following stimulation with light, the dye absorbance, measured at the Ca-sensitive wavelength pair 660-690 nm increased and remained elevated for 10s of seconds. The absorbance change began during the initial part of the photodepolarization, but the early time course was obscured by the stimulus flash. Absorbance at a second wavelength pair, 630-690 nm, changed only a small amount during the photoresponse. This wavelength dependence of the dye absorbance was the same as that observed for direct Ca injections into larger Hermissenda neurons. Pairing the light stimulus with depolarizing current (0.5 nA) increased the dye absorbance, while sufficient hyperpolarizing current (0.5-1 nA) markedly reduced the dye response to a paired light flash. Depolarizing current alone gave a small, slowly rising dye absorbance change. Light- and current-induced dye absorbance change was greatly reduced by external Cd. We conclude that light stimulus causes an increase in cytoplasmic Ca, which is accentuated by extrinsic depolarizing input, and that most of the increase results from transmembrane influx.

1965 ◽  
Vol 48 (5) ◽  
pp. 841-858 ◽  
Author(s):  
J. V. Milligan

Using area under the contracture curve to quantitate contractures, the diffusion coefficient of calcium ions within the frog toe muscle during washout in a calcium-free solution and subsequent recovery after reintroduction of calcium to the bathing solution was calculated to be about 2 x 10-6 cm2/sec. The diffusion coefficient measured during washout was found to be independent of temperature or initial calcium ion concentration. During recovery it was found to decrease if the temperature was lowered. This was likely due to the repolarization occurring after the depolarizing effect of the calcium-free solution. The relation between contracture area and [Ca]o was found to be useful over a wider range than that between maximum tension and [Ca]o. The normalized contracture areas were larger at lower calcium concentrations if the contractures were produced with cold potassium solutions or if NO3 replaced Cl in the bathing solutions. Decreasing the potassium concentration of the contracture solution to 50 mM from 115 mM did not change the relation between [Ca]o and the normalized area. If the K concentration of the bathing solution was increased, the areas were decreased at lower concentrations of Ca.


1991 ◽  
Vol 69 (10-11) ◽  
pp. 722-727 ◽  
Author(s):  
Marta S. Fernández ◽  
Ricardo Mejía ◽  
Eunice Zavala

Analysis of the time course of hydrolysis of dimyristoylphosphatidylcholine liposomes catalyzed by porcine pancreatic phospholipase A2 at 18 °C shows that, in the presence of 10 mM NaCl, the length of the latency period in the presteady-state phase increases from 3 to 10.5 min when the CaCl2 concentration is reduced from 15 to 1 mM. This inverse dependence of the lag period on calcium ion concentration is seen more readily at 1 M NaCl, where the induction time changes from 13.5 to 42 min by decreasing the concentration of CaCl2 from 15 to 1 mM. To interpret these results, we took into account the small amount of fatty acid that is produced during the latency phases. The fatty acid generates a negative surface electrostatic potential and makes the interfacial concentration of calcium ions different from the concentration in the bulk solvent. Variations in the analytical concentrations of NaCl and CaCl2 affect both the interfacial calcium ion concentration and electrostatic potential, as estimated theoretically from Grahame and Boltzmann equations. According to these estimates, the length of the latency period diminishes with the increase of the interfacial calcium concentration, but does not show any logical dependence on the change in surface electrostatic potential.Key words: phospholipase A2, latency phase, interfacial calcium ion concentration, liposomes.


1999 ◽  
Vol 81 (4) ◽  
pp. 1587-1596 ◽  
Author(s):  
B. Maya Kato ◽  
Edwin W Rubel

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.


Geosciences ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 187
Author(s):  
Rolf Vieten ◽  
Francisco Hernandez

Speleothems are one of the few archives which allow us to reconstruct the terrestrial paleoclimate and help us to understand the important climate dynamics in inhabited regions of our planet. Their time of growth can be precisely dated by radiometric techniques, but unfortunately seasonal radiometric dating resolution is so far not feasible. Numerous cave environmental monitoring studies show evidence for significant seasonal variations in parameters influencing carbonate deposition (calcium-ion concentration, cave air pCO2, drip rate and temperature). Variations in speleothem deposition rates need to be known in order to correctly decipher the climate signal stored in the speleothem archive. StalGrowth is the first software to quantify growth rates based on cave monitoring results, detect growth seasonality and estimate the seasonal growth bias. It quickly plots the predicted speleothem growth rate together with the influencing cave environmental parameters to identify which parameter(s) cause changes in speleothem growth rate, and it can also identify periods of no growth. This new program has been applied to multiannual cave monitoring studies in Austria, Gibraltar, Puerto Rico and Texas, and it has identified two cases of seasonal varying speleothem growth.


SIMULATION ◽  
1979 ◽  
Vol 32 (6) ◽  
pp. 193-204 ◽  
Author(s):  
George G. Járos ◽  
Thomas G. Coleman ◽  
Arthur C. Guyton

1991 ◽  
Vol 97 (6) ◽  
pp. 1165-1186 ◽  
Author(s):  
R Payne ◽  
B V Potter

Limulus ventral photoreceptors contain calcium stores sensitive to release by D-myo-inositol 1,4,5 trisphosphate (InsP3) and a calcium-activated conductance that depolarizes the cell. Mechanisms that terminate the response to InsP3 were investigated using nonmetabolizable DL-myo-inositol 1,4,5 trisphosphorothioate (InsPS3). An injection of 1 mM InsPS3 into a photoreceptor's light-sensitive lobe caused an initial elevation of cytosolic free calcium ion concentration (Cai) and a depolarization lasting only 1-2 s. A period of densensitization followed, during which injections of InsPS3 were ineffective. As sensitivity recovered, oscillations of membrane potential began, continuing for many minutes with a frequency of 0.07-0.3 Hz. The activity of InsPS3 probably results from the D-stereoisomer, since L-InsP3 was much less effective than InsP3. Injections of 1 mM InsP3 caused an initial depolarization and a period of densensitization similar to that caused by 1 mM InsPS3, but no sustained oscillations of membrane potential. The initial response to InsPS3 or InsP3 may therefore be terminated by densensitization, rather than by metabolism. Metabolism of InsP3 may prevent oscillations of membrane potential after sensitivity has recovered. The InsPS3-induced oscillations of membrane potential accompanied oscillations of Cai and were abolished by injection of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid. Removal of extracellular calcium reduced the frequency of oscillation but not its amplitude. Under voltage clamp, oscillations of inward current were observed. These results indicate that periodic bursts of calcium release underly the oscillations of membrane potential. After each burst, the sensitivity of the cell to injected InsP3 was greatly reduced, recovering during the interburst interval. The oscillations may, therefore, result in part from a periodic variation in sensitivity to a constant concentration of InsPS3. Prior injection of calcium inhibited depolarization by InsPS3, suggesting that feedback inhibition of InsPS3-induced calcium release by elevated Cai may mediate desensitization between bursts and after injections of InsPS3.


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