Mobilization of Intracellular Calcium by the General Anaesthetic Halothane in Cultured, Identified Molluscan Neurons
22 Jul 2020-Vol. 12, Iss: 8, pp 90-100
About: The article was published on 2020-07-22 and is currently open access. It has received 4 citations till now. The article focuses on the topics: General anaesthetic & Halothane.
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TL;DR: Using the two electrode voltage clamp configuration, a high voltage activated whole-cell Ca2+ channel current (IBa) was recorded from a cluster of neurosecretory ‘Light Yellow’ Cells (LYC) in the right parietal ganglion of the pond snail Lymnaea stagnalis, showing a reversible concentration-dependent depression of current amplitude in the presence of the volatile anaesthetics halothane, isoflurane and sevofl Lurane.
Abstract: O_LIUsing the two electrode voltage clamp configuration, a high voltage activated whole-cell Ca2+ channel current (IBa) was recorded from a cluster of neurosecretory Light Yellow Cells (LYC) in the right parietal ganglion of the pond snail Lymnaea stagnalis. C_LIO_LIRecordings of IBa from LYCs show a reversible concentration-dependent depression of current amplitude in the presence of the volatile anaesthetics halothane, isoflurane and sevoflurane, or the non-volatile anaesthetic pentobarbitone at clinical concentrations. C_LIO_LIIn the presence of the anaesthetics investigated, IBa measured at the end of the depolarizing test pulse showed proportionally greater depression than that at measured peak amplitude, as well as significant decrease in the rate of activation or increase in inactivation or both. C_LIO_LIWithin the range of concentrations used, the concentration-response plots for all the anaesthetics investigated correlate strongly to straight line functions, with linear regression R2 values > 0.99 in all instances. C_LIO_LIFor volatile anaesthetics, the dose-response regression slopes for IBa increase in magnitude, in order of gradient: sevoflurane, isoflurane and halothane, a sequence which reflects their order of clinical potency in terms of MAC value. C_LI
5 citations
Cites background from "Mobilization of Intracellular Calci..."
...volatile anaesthetics has been shown in CA1 hippocampal cells in rats [1] and cultured molluscan neurons in the absence of extracellular Ca2+[2,3], implying an anaesthetic triggered release of Ca2+ from intracellular stores....
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01 Jan 2015
TL;DR: Ketamine protects isolated rabbit ventricular myocytes against [Ca2+]i overload by inhibiting INaL and ICaL in a concentration-dependent manner.
Abstract: Aim:Intracellular Ca2+ ([Ca2+]i) overload occurs in myocardial ischemia. An increase in the late sodium current (INaL) causes intracellular Na+ overload and subsequently [Ca2+]i overload via the reverse-mode sodium-calcium exchanger (NCX). Thus, inhibition of INaL is a potential therapeutic target for cardiac diseases associated with [Ca2+]i overload. The aim of this study was to investigate the effects of ketamine on Na+-dependent Ca2+ overload in ventricular myocytes in vitro.Methods:Ventricular myocytes were enzymatically isolated from hearts of rabbits. INaL, NCX current (INCX) and L-type Ca2+ current (ICaL) were recorded using whole-cell patch-clamp technique. Myocyte shortening and [Ca2+]i transients were measured simultaneously using a video-based edge detection and dual excitation fluorescence photomultiplier system.Results:Ketamine (20, 40, 80 μmol/L) inhibited INaL in a concentration-dependent manner. In the presence of sea anemone toxin II (ATX, 30 nmol/L), INaL was augmented by more than 3-fold, while ketamine concentration-dependently suppressed the ATX-augmented INaL. Ketamine (40 μmol/L) also significantly suppressed hypoxia or H2O2-induced enhancement of INaL. Furthermore, ketamine concentration-dependently attenuated ATX-induced enhancement of reverse-mode INCX. In addition, ketamine (40 μmol/L) inhibited ICaL by 33.4%. In the presence of ATX (3 nmol/L), the rate and amplitude of cell shortening and relaxation, the diastolic [Ca2+]i, and the rate and amplitude of [Ca2+]i rise and decay were significantly increased, which were reverted to control levels by tetrodotoxin (TTX, 2 μmol/L) or by ketamine (40 μmol/L).Conclusion:Ketamine protects isolated rabbit ventricular myocytes against [Ca2+]i overload by inhibiting INaL and ICaL.
3 citations
30 Sep 2020
TL;DR: This study highlights the need to understand more fully the role of environmental factors in the development of Alzheimer's disease and how these factors are influenced by age and disease progression.
Abstract: 1Physology Research Centre, Department of Physiology, School of Medicine, Ahwaz Jundishapur University of Medical Sciences, Ahwaz, Iran 2Dipartimento di Biologia, Università Degli Studi di Napoli Federico II, Napoli, Italy 3Institute of Ageing and Chronic Diseases, The APEX building, University of Liverpool, UK *Corresponding Author: William Winlow, Dipartimento di Biologia, Università Degli Studi di Napoli Federico II, Napoli, Italy and Institute of Ageing and Chronic Diseases, The APEX building, University of Liverpool, UK.
2 citations
Cites background or methods from "Mobilization of Intracellular Calci..."
...Intracellular calcium imaging with Fura-2-Individual neurons were loaded with the cell-permeable ratiometric Ca2+ indicator Fura2 acetoxymethyl ester (Fura-2 AM) as previously described [40-42]....
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...However, as with NO and H202, we have previously demonstrated that a number of substances can increase [Ca]i in Lymnaea neurones; these include volatile anesthetics [35,42], caffeine [40 ] and ryanodine [41]....
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30 Jun 2020
2 citations
References
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TL;DR: It is proposed that, depending on its Ca2+ content, the caffeine‐sensitive store can either attenuate or potentiate responses to depolarization.
Abstract: 1. We studied how in changes in cytosolic free Ca2+ concentration ([Ca2+]i) produced by voltage-dependent Ca2+ entry are influenced by a caffeine-sensitive Ca2+ store in bullfrog sympathetic neurones. Ca2+ influx was elicited by K+ depolarization and the store was manipulated with either caffeine or ryanodine. 2. For a time after discharging the store with caffeine and switching to a caffeine-free medium: (a) [Ca2+]i was depressed by up to 40-50 nM below the resting level, (b) caffeine responsiveness was diminished, and (c) brief K+ applications elicited [Ca2+]i responses with slower onset and faster recovery than controls. These effects were more pronounced as the conditioning caffeine concentration was increased over the range 1-30 mM. 3. [Ca2+]i, caffeine and K+ responsiveness recovered in parallel with a half-time of approximately 2 min. Recovery required external Ca2+ and was speeded by increasing the availability of cytosolic Ca2+, suggesting that it reflected replenishment of the store at the expense of cytosolic Ca2+. 4. During recovery, Ca2+ entry stimulated by depolarization had the least effect on [Ca2+]i when the store was filling most rapidly. This suggests that the effect of Ca2+ entry on [Ca2+]i is modified, at least in part, because some of the Ca2+ which enters the cytosol during stimulation is taken up by the store as it refills. 5. Further experiments were carried out to investigate whether the store can also release Ca2+ in response to stimulated Ca2+ entry. In the continued presence of caffeine at a low concentration (1 mM), high K+ elicited a faster and larger [Ca2+]i response compared to controls; at higher concentrations of caffeine (10 and 30 mM) responses were depressed. 6. Ryanodine (1 microM) reduced the rate at which [Ca2+]i increased with Ca2+ entry, but not to the degree observed after discharging the store. At this concentration, ryanodine completely blocked responses to caffeine but had no detectable effect on Ca2+ channel current or the steady [Ca2+]i level achieved during depolarization. 7. We propose that, depending on its Ca2+ content, the caffeine-sensitive store can either attenuate or potentiate responses to depolarization. When depleted and in the process of refilling, the store reduces the impact of Ca2+ entry as some of the Ca2+ entering the cytosol during stimulation is captured by the store.(ABSTRACT TRUNCATED AT 400 WORDS)
282 citations
TL;DR: A structural understanding of this mechanism will provide a framework for understanding the regulation of Ca2+ entry and accumulation in neurons.
Abstract: Calcium ions are ubiquitous intracellular mediators of numerous cellular processes. One of the main mechanisms of Ca2+ entry into the cell involves the opening of Ca2+ channels in the plasma membrane. To effectively control Ca2+ signalling, Ca2+ channels inactivate rapidly by a mechanism that depends on an elevation of intracellular Ca2+ within tens of nanometres of the channel pore. A structural understanding of this mechanism will provide a framework for understanding the regulation of Ca2+ entry and accumulation in neurons. Recent physiological, biochemical and molecular studies have yielded new insights into the regulation of neuronal Ca2+ channels.
222 citations
"Mobilization of Intracellular Calci..." refers background in this paper
...But in fact this reported probability of Ca2+ channels blockage or depression of Ca2+ currents by halothane [7,10,34] might well be a reflection of halothane-induced elevation in [Ca]i which mediates calcium-dependent inactivation of Ca2+ channels [10,35]....
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TL;DR: In this article, the distribution and actions of three spontaneously occurring wide-acting synaptic inputs on identified neurons of the visceral and right parietal ganglia of Lymnaea stagnalis are described.
175 citations
TL;DR: The findings suggest that the negative inotropic and chronotropic actions of halothane, enflurane, and isoflurane on the ventricular myocardium are related, at least in part, to their inhibition of ICa at the sarcolemma.
Abstract: The effects of halothane, enflurane, and isoflurane on voltage-dependent Ca2+ channel current (ICa) were compared in canine ventricular cells by the whole-cell voltage-clamp technique. ICa was elicited in each cell by progressively depolarizing pulses, from - 80 or −40 m V to more positive membrane
140 citations
"Mobilization of Intracellular Calci..." refers result in this paper
...Similar results have also been reported in recombinant cardiac L-type channels expressed in human embryonic kidney cells (HEK293) [8], cultured neocortical astrocytes [9], cortical area 1 (CA1) neurons in hippocampal slices [10] clonal pituitary cells [11,12], isolated chromaffin cells [13-15], rat pheochromocytoma (PC12) cells [16] Xenopus oocytes [17], human neuronal cell lines [18], guinea pig myocytes [19], rabbit myocardial cells [20] and dogs [21,22]....
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133 citations
"Mobilization of Intracellular Calci..." refers background in this paper
...Cell calcium pumps maintain a large inward calcium gradient into cells and in most cytosols the level of free calcium oscillates between 0.1 and 0.2 µM according to Carafoli [37], but occurs in millimolar concentrations in extracellular fluid of vertebrates and also in Lymnaea stagnalis [38], our chosen model preparation....
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...2 μM according to Carafoli [37], but occurs in millimolar concentrations in extracellular fluid of vertebrates and also in Lymnaea stagnalis [38], our chosen model preparation....
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