The Effect Of H2s On Ion Currents Biology Essay
The chief end of this survey was to look into the consequence of H2S on ion currents and membrane potencies of Helix pomatia U-cells. H2S is by and large known as a really toxic gas but the comparatively high degrees of 50-160 Aµmol/l H2S in mammalian encephalon tissue ( Savage & A ; Gould, 1990 ; L R Goodwin et al. , 1989 ; Marcus W. Warenycia et al.
, 1989 ) and the physiological maps of H2S like synaptic transition, vasorelaxation and neuroprotection ( reviewed by A?owicka & A ; BeA‚towski, 2007 and Mancardi et al. , 2009 ) suggest an of import function as gaseous signaling molecule. As reviewed in Wang ( 2002 ) it is hypothesized that H2S is the 3rd gasotransmitter beside CO and NO. H2S acts on many marks including ion channels such as K and Ca channels ( Kawabata et al. , 2007 ; W. Yang et al. , 2005 ; Zhao & A ; Rui Wang, 2002 ; Zhao et al.
, 2001 ; Sitdikova et al. , 2010 ) . The research on physiological effects of H2S on ion channels increases our cognition about the map of gasotransmitters in invertebrates and craniates.In the present survey NaHS was used as a H2S giver and applied extracellularly to the ganglia. NaHS was normally used at a concentration of 100 AµM in the experiments, whereas at a physiological pH of 7.4 about one tierce of H2S is present in the undissociated signifier and the staying two 3rd exist in HS- ( R J Reiffenstein et al. , 1992 ) .
The concentration of about 30 Aµmol/l H2S, which is efficaciously in the solution, is even below the scope of 50-160 Aµmol/l detected in mammalian encephalon tissue ( Savage & A ; Gould, 1990 ; L R Goodwin et al. , 1989 ; Marcus W. Warenycia et al. , 1989 ) and similar to the reported plasma degrees of 34 Aµmol/l H2S in mice and 44 Aµmol/l H2S in worlds ( Li et al. , 2005 ) .
The influence of 100 AµM Na+ on the electrophysiological experiments is negligible, because the bath solution for controls contains 80 mmol/l of Na+ . NaHS besides does n’t act upon the pH of the bath solution at concentrations of & lt ; 1mmol/l NaHS ( Hideo Kimura et al. , 2005 ) .
In the present survey an addition in the K outward currents after extracellular application of 100 AµM NaHS was found. This consequence was smaller in Ca2+-free solution. NaHS shifted the I-V curve of K outward currents to the left on the electromotive force axis. 100 AµM NaHS significantly ( p & lt ; 0.05 ) decreased the Ca inward current and changed the activation and inactivation dynamicss of Ca2+ channels. I„ of activation kinetic was significantly ( p & lt ; 0.05 ) decreased and I„ of inactivation dynamicss was increased by NaHS.
100 AµM NaHS acted on firing cells in many ways and changed the action possible clip class in current clinch experiments. The membrane potency was depolarized significantly ( p & lt ; 0.05 ) and the action possible amplitude was significantly ( p & lt ; 0.05 ) decreased. The action possible rise incline and maximal rise incline every bit good as decay incline and maximal decay incline are decreased under NaHS status ( all differences are important except rise incline ) .
Action possible rise clip and decay clip are significantly ( p & lt ; 0.05 ) increased compared to command conditions. The action possible half-width, which is a measuring of the action possible continuance at half of the amplitude, is prolonged by NaHS.One of the most conspicuous effects of 100 Aµmol/l NaHS in the experiments was the addition of potassium outward currents in electromotive force clinch experiments, with a half maximal concentration of 49.81 A± 7.41 Aµmol/l NaHS. This shows that H2S induces effects on the outward currents even below the ascertained physiological relevant concentration of 50-160 Aµmol/l ( Savage & A ; Gould, 1990 ; L R Goodwin et al.
, 1989 ; Marcus W. Warenycia et al. , 1989 ) .
The comparatively steep dose-response curve illustrates the narrow scope of the physiological H2S consequence. At concentrations of 1 mmol/l the consequence of H2S on the outward current was already reduced to 70 A± 7.81 % of the full consequence. In experiments on hippocampal pieces in rats, endogenous H2S degrees of 50-160 Aµmol/l have been shown to ease the long term potentiation ( LTP ) .
But H2S concentrations of 320 and 640 Aµmol/l suppressed field EPSPs and population spikes and no consequence was observed ( Abe & A ; H Kimura, 1996 ) . Furthermore, deadly H2S concentration in the encephalon of rats is merely 2-fold ( ! ) higher than endogenous degrees of H2S ( Marcus W. Warenycia et al. , 1989 ) . A little scope of H2S consequence on formation of memory was besides observed in the snail Lymnaea stagnalis. Exposure to 75 and 100 Aµmol/l showed an consequence on acquisition and memory formation, whereas 50 Aµmol/l H2S showed no consequence ( Rosenegger et al. , 2004 ) .H2S shifts the I-V curve of outward currents to the left, which indicates that ion channels activate at lower membrane potencies.
The I-V relationship shows that outward currents at physiological membrane potencies ( V = & lt ; +50 millivolt ) are increased by H2S. In spot clinch and whole cell experiments it has been demonstrated that the outward current in U-cells flows chiefly through BK-type Ca2+ activated K+ channels ( Gola et al. , 1990 ) . The ascertained addition of K+ outward current below +50 millivolt caused by H2S lucifers with the scope where the BK-type current is prevailing, doing the BK-type channels a possible mark of H2S. A fast energizing and demobilizing K outward current besides referred to as transeunt outward K+-current ( IK ( A ) ) has been discovered in invertebrate and craniate cells ( Connor & A ; C F Stevens, 1971 ; Rogawski, 1985 ; Y.
Nakajima et al. , 1986 ) and was found in medium sized Helix nerve cells ( Erwin Neher, 1971 ; Kiss et al. , 2002 ) .
However IK ( A ) has non been reported to be outstanding in U-cells. The presence of the IK ( A ) and delayed outward current are indicated by an initial rapid rise in the outward current, which consequences in a alteration from a fast to a slow rise. Experiments on U-cells where different depolarizing pulsations were delivered ( +20 to +120 millivolt ) ( informations non shown ) reveal a really little alteration in the clip class of the outward currents compared to other cells in Helix pomatia. This suggests that this current constituent makes merely a minor part to the entire current. In experiments conducted by Lux and Hofmeier ( 1982 ) these fast energizing currents were determined by the amplitude of the current at the point of the maximal alteration in the current clip class.
The mensural current values at this point contribute less than 7 % to the entire outward current during a depolarizing pulsation. Furthermore a fast outward current was found in U-cells and was attributed to voltage dependent K+-channels ( KV channels ) . But in U-cells the KV constituent was merely noticeable at big depolarisations, and in the physiological scope at electromotive forces lower than +40 millivolt this constituent contributed less than 10 % to the net outward current. It was found that KV channels played a limited function in U-cells ( Crest & A ; Gola, 1993 ) and the outward current in U-cells consists about entirely of Ca2+ mediated K+ outward current ( H D Lux & A ; Hofmeier, 1982 ) . These findings strongly suggest that BK-type channels are involved in the increased outward current caused by H2S.
Intracellular buffering of Ca2+ by dibromo-BAPTA abolished the N-shape in the IV curve of outward currents and the H2S evoked addition of outward currents below +50 millivolt. These facts besides suggest that BK-type channels play a function in the outward current increasing consequence of H2S. A recent spot clinch survey carried out by Sitdikova et Al. ( 2010 ) supports this premise.
H2S enhanced the activity of BK channels in rat pituitary tumour cells by increasing the channel unfastened chance.As shown in the I-V curve the outward currents above +120 millivolt are every bit good increased by H2S. The addition of outward currents above +120 millivolt was non abolished after injection of dibromo-BAPTA, which buffered intracellular Ca2+ . But the increased activation of the BK-type channels could account for this consequence above +120 millivolt every bit good.
It was found that the activation of hSlo ( BK channel in human cells ) becomes independent below intracellular Ca2+ concentration of 100 nmol/l and activates at +200 millivolt ( Vergara et al. , 1998 ) . It is possible that BK-type channels in Helix pomatia above +120 millivolt activate in the absence of intracellular Ca2+ and are involved in the increasing consequence of H2S on the outward current above +120 millivolt.
H2S could besides increase the KV current constituent above +120 millivolt. Further experiments are required to look into which current constituents are responsible for the increased outward current above +120 millivolt.Using CP 339818 hydrochloride, a Kv1.3 and Kv1.4 K+ channel blocker, reduced the K+ outward current merely in some cells. In these cells H2S still increased the outward currents, which leads to the premise that the consequence of H2S is non carried by KV channels to a big extent.
But in some cells H2S had no consequence after perfusion with CP 339818 hydrochloride. In cells where CP 339818 hydrochloride had a little or no consequence the addition of the outward current after NaHS application was comparatively high. This could hold different grounds: ( 1 ) CP 339818 hydrochloride did n’t barricade KV channels wholly and hence NaHS could trip these channels which would do the addition in outward current.
( 2 ) Cells which were non or to a little extent affected by CP 339818 hydrochloride had a comparatively little figure of KV-channels and big figure of BK-type channels and the latter would do the addition in outward current after NaHS application. The fact that KV channels contribute merely 10 % to the outward current at electromotive forces below +40 millivolt ( Crest & A ; Gola, 1993 ) , instead suggests the 2nd possibility.In electromotive force clinch experiments Ca2+-free solution reduced the entire outward current, which suggests that Ca2+ activated K+ currents are reduced in Ca2+ free medium. This premise is strengthened by the determination that Ca2+-free bath solution suppresses Ca2+ activated K+ current in U-cells ( H D Lux & A ; Hofmeier, 1982 ) . In Ca free solution H2S increases the outward currents merely to 124 % , whereas in control bath solution ( incorporating Ca2+ ) H2S increases the outward current to 178 % . Therefore, the increasing consequence of H2S on the outward currents is reduced to 31 % compared to the consequence in normal bath solution. Therefore proposing that reduced Ca2+-activated K+-currents cause a strong lessening of the H2S consequence, bespeaking an of import function of BK-type channels in the consequence of H2S.
These consequences may raise the inquiry why the outward current was n’t wholly blocked by Ca2+-free solution. Since a little sum of the outward current in U-cells is ascribed to the KV current, the staying outward current could be ascribed to the KV current, which does non peculiarly depend on extracellular Ca2+ ( Heyer & A ; H D Lux, 1976 ) . Given that H2S increased the staying current constituent in Ca2+ free status, the increased outward current could so be ascribed partially to an addition of the KV current constituent. Furthermore, a nominally Ca2+ free solution still contains some Ca2+ ( H D Lux & A ; Hofmeier, 1982 ) , possibly forestalling a complete blocking of Ca2+ activated K+ current. Further experiments are necessary to happen out to which extent BK-type channels and KV channels are involved in the consequence of H2S.
In spot clinch surveies on Helix U-cells it was found that Ca2+-activated K+-channels have to be colocalized with Ca2+ channels to be involved in fire of nervus cells. Furthermore the Ca2+-activated K+-channels did non open if related Ca2+ channels were prevented from opening ( Gola & A ; Crest, 1993 ) . These consequences indicate a strong functional relationship between Ca2+-activated K+-channels and Ca2+-channels. Therefore one could presume that a possible addition of Ca2+-inward current caused by H2S, which would accordingly take to enhanced activation of Ca2+ activated K+ channels, could take to an increased outward current.
But experiments of the present survey in Na+-free solution incorporating the K+-channel blockers TEA and 4-AP, showed a lessening of the HVA Ca2+ inward current in H2S conditions. The lessening of HVA Ca2+-current by 15 % regulations out the hypothesis that an addition in Ca2+ inward current is responsible for the increased K+ outward current. Though the I-V curve shows an addition of the HVA Ca2+-current at 0 millivolt in H2S status, it is assumed that this consequence is non responsible for the mensural addition of outward current. In electromotive force clinch experiments the cells were normally depolarized to +20 millivolt, and at this possible the HVA Ca2+-current was decreased by H2S as it is shown in the I-V curve of HVA Ca2+-currents. An repressive consequence of H2S on L-type Ca2+ channels was besides found in cardiomyocytes of rats ( Sun et al.
, 2008 ) . In this survey it was observed that the recovery from depolarization-induced inactivation was inhibited by NaHS. No displacement of the HVA Ca2+-current I-V curve was found after NaHS intervention in our survey, which is in line with the findings of Sun et Al.
( 2008 ) . This suggests that the electromotive force dependance of HVA Ca2+ channels was non modified by an interaction with H2S.A survey carried out on astrocytes showed that H2S induces Ca2+ waves chiefly through an addition of Ca2+ inflow ( NAGAI et al. , 2004 ) . This determination seems to be contradictory to the ascertained lessening of HVA Ca2+ channels in the present survey. However the type of Ca2+ channel, which was affected by H2S in astrocytes was non determined.
Therefore it can be assumed that in mammalian astrocytes a different type of Ca2+ channel was affected by H2S than in the mollusk U-cell of Helix pomatia. Exposure of cerebellar granule nerve cells to H2S for two hours raises cytosolic Ca2+ through activation of L-type Ca2+ channels ( Garcia-Bereguiain et al. , 2008 ) . But in mollusks L-type like Ca2+ channels were found to hold different belongingss ( conductance, sensitiveness to blockers, activation ) ( Kits & A ; Mansvelder, 1996 ) , and it can be assumed that H2S affects Ca2+ channels in Helix pomatia in a different manner.By using curve adjustment to the HVA Ca2+ inward current it was found that H2S decreases the activation clip of the current. aˆ¦aˆ¦.
Hier sollte noch Text hinzukommen, sobald ich Artikel von der Bibliothek erhalten habe.In order to look into the consequence of H2S in physiological conditions, current clinch experiments were carried out. H2S reduced the amplitude of action potencies and changed the clip class. In control bath solution the action possible wave-off peaked at +46.4 A± 2.33 millivolt, which is similar to the wave-off of +42 millivolt found in a old survey ( Crest & A ; Gola, 1993 ) . Cell free individual channel recordings in changeless Ca2+ concentration suggest that the H2S consequence on BK channels is independent of the external Ca2+ inflow ( Sitdikova et al.
, 2010 ) . Given that no Ca2+ inflow is necessary for the H2S consequence on BK channels, a changeless modulating of BK type channels by H2S can be assumed. This presumptively leads to activation at lower membrane potencies, which is supported by the displacement of the I-V current to the left. An activation of BK-type channels at lower potencies would overlap the inward current and accordingly lead to a reduced net inward current during the action possible wave-off. This is in line with the determination that the Ca2+-activated K+ current overlaps the Ca2+ inward current during spike explosion and leads to a decrease of the depolarizing inclination ( Crest & A ; Gola, 1993 ) . A lessening of action possible amplitude by H2S was besides obtained in a survey carried out in rat atrial myocardium ( Abramochkin et al.
, 2009 ) . H2S changed the electrical activity by diminishing the action possible clip class and amplitude. Furthermore 500 AµM NaHS caused a depression of electrical activity after 4 min. of perfusion.
This fits the consequences of our survey, where a depression of firing activity was besides observed in three out of four experiments after 6.4 A± 2.8 min. Activation of BK-type channels could be a possible account for this consequence every bit good.
Overlaping of a invariably increasing Ca2+-activated K+ current with the Ca2+ inward current was observed to do a halt in firing activity of U-cells ( Crest & A ; Gola, 1993 ) .It is besides really likely that the ascertained lessening of Ca2+ current reduces the action possible amplitude. Since the inward current is chiefly carried by Ca2+ in U-cells and the action potencies are considered as Ca2+ spikes ( Gola et al. , 1990 ; H D Lux & A ; Hofmeier, 1982 ; Crest & A ; Gola, 1993 ) , it is really likely that the lessening of the HVA Ca2+ current is involved in the decrease of the action possible amplitude after NaHS perfusion.The action possible rise clip and the action possible decay clip was increased by H2S taking to a wider action potency, which besides becomes evident in the increased half-width clip. Assuming an activation of BK-type channels by H2S a decreased continuance of action potencies could be expected, which was already observed in rat atrial myocardium ( Abramochkin et al. , 2009 ) . Further surveies are required to happen out which affect causes the increased half-width clip of action potencies in Helix pomatia U-cells.
In farther analysis a maximal rise incline of 14.35 A± 1.66 V/s was observed, which is similar to the rise incline of 13.5 V/s found by Crest & A ; Gola ( 1993 ) .
H2S decreased the maximal rise incline to 8.62 A± 1.54 V/s. Given that the maximal rise incline of the action potency is relative to the inward current ( Hodgkin & A ; Katz, 1949 ) , the reduced Ca2+ current presumptively leads to a lower rise incline. Furthermore an addition of BK-type channel activity could besides ensue in a decreased net outward current which would take to a decreased rise incline. It was observed that BK-type channels open a few msecs after the spike wave-off ( Gola et al.
, 1990 ) . But BK-type channels likely activate earlier in H2S conditions, and hence could impact the rise incline.The ascertained maximal decay incline of 6.93 A± 0.80 V/s was found to be similar to 8.
8 V/s obtained by Crest & A ; Gola ( 1993 ) . H2S decreased the maximal decay incline to 4.02 A± 0.63 V/s. Further surveies are needed to look into which consequence leads to the decreased action potency decay clip and decay incline.BK-type channels show a fast electromotive force dependance.
BK-type K+ currents last a few 10s of msecs after the action potency and it is assumed that these channels are non straight involved in defining of interspike flight ( Lancaster et al. , 1991 ) . Therefore BK-type K+ channels are presumptively non involved in the depolarising consequence of H2S on the membrane potency. Furthermore activation of BK channels by H2S would take to a hyperpolarization of the membrane potency. A lessening of the K+ outward current at the resting potency is one possible account that could take to a depolarisation of the membrane potency by H2S. But no lessening of the outward current was observed at resting potencies in the I-V curves by H2S, which could supply an account for the depolarising consequence of H2S on the membrane potency. Since Ca2+ inward currents are non activated at membrane potencies below -20 millivolt, it can be ruled out that an addition of this current histories for the depolarizing consequence. The ground for the depolarized resting potency remains to be determined and further current clinch and electromotive force clinch experiments are needed to look into this consequence.
The consequences strongly suggest an actuating consequence of H2S on BK-type channels. Given that H2S is a cut downing agent the modulating consequence on BK channels is linked to the cut downing action on proteins. BK channel activity is increased by cut downing agents in different cell types like human embryologic kidney 293 cells ( DiChiara & A ; Reinhart, 1997 ) , CA1 pyramidal nerve cells from grownup rat hippocampus ( Gong et al. , 2000 ) , myocytes from coney pneumonic arteria ( Thuringer & A ; Findlay, 1997 ) and smooth musculus cells ( Zhao-Wen Wang et al. , 1997 ) . This is supported by the determination that Dithiothreitol ( DTT ) itself increases the unfastened chance ( Popen ) of BK channels but abolishes the H2S consequence on BK channels, whereas the oxidising agent sodium ethylmercurithiosalicylate reduces Popen of BK channels without suppressing the H2S consequence ( Sitdikova et al. , 2010 ) . BK channel activity is modulated by DTT and sodium ethylmercurithiosalicylate merely when applied to the intracellular side of the spot ( Zhao-Wen Wang et al.
, 1997 ) , proposing that the cysteine residue which is responsible for the oxidation-reduction transition ( Erxleben et al. , 2002 ) , is on the intracellular side of the ion channel. In the experiments of the present survey NaHS was applied extracellularly, but since H2S is non charged and easy permeates cell membranes, presumptively it acts from the cytosolic side on BK-type channels.
BK channel activity is modulated by the redox province of critical sulfhydryl groups, located in the channel protein or an associated regulative protein ( DiChiara & A ; Reinhart, 1997 ; Z W Wang et al. , 1997 ) .In drumhead, the present survey demonstrates that H2S increases the K outward current, whereas BK-type channels are really likely to lend to this consequence. Furthermore the HVA Ca2+ current is decreased and the activation and inactivation clip is changed by H2S. These alterations in inward every bit good as in outward currents, eventually lead to a alteration in the fire activity of U-cells. It can be assumed that the decreased action possible amplitude, the changed clip class of action potencies and the depolarized membrane potency have physiological effects.
A nexus of electrical activity and H2S was besides found in a survey carried out on mice. H2S production was found to be enhanced by nervous excitement and by the excitant neurotransmitter L-glutamate. Furthermore long term potentiation ( LTP ) is altered in cystathionine I?-synthase ( CBS ) knock-out mice and hence H2S may modulate synaptic activity ( Eto et al. , 2002 ) .
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