scholarly journals Hyperpolarisation-activated calcium currents found only in cells from the elongation zone of Arabidopsis thaliana roots

2000 ◽  
Vol 21 (2) ◽  
pp. 225-229 ◽  
Author(s):  
Ed Kiegle ◽  
Matt Gilliham ◽  
Jim Haseloff ◽  
Mark Tester
2014 ◽  
Vol 70 (3) ◽  
pp. 187-198
Author(s):  
Ewa Kupidłowska

The ultrastructure and morphology of roots treated with coumarin and umbelliferone as well as the reversibility of the coumarins effects caused by exogenous GA, were studied in <em>Arabidopsis thaliana</em>. Both coumarins suppressed root elongation and appreciably stimulated radial expansion of epidermal and cortical cells in the upper part of the meristem and in the elongation zone. The gibberellic acid applied simultaneously with coumarins decreased their inhibitory effect on root elongation and reduced cells swelling.Microscopic observation showed intensive vacuolization of cells and abnormalities in the structure of the Golgi stacks and the nuclear envelope. The detection of active acid phosphatase in the cytosol of swollen cells indicated increased membrane permeability. Significant abnormalities of newly formed cell walls, e.g. the discontinuity of cellulose layer, uncorrect position of walls and the lack of their bonds with the mother cell wall suggest that coumarins affected the cytoskeleton.


2011 ◽  
Vol 106 (5) ◽  
pp. 2486-2498 ◽  
Author(s):  
Wen-hsin Ku ◽  
Stephen P. Schneider

Whole cell patch-clamp recordings were used to investigate the contribution of transient, low-threshold calcium currents ( IT) to firing properties of hamster spinal dorsal horn neurons. IT was widely, though not uniformly, expressed by cells in Rexed's laminae I–IV and correlated with the pattern of action potential discharge evoked under current-clamp conditions: IT in neurons responding to constant membrane depolarization with one or two action potentials was nearly threefold larger than IT in cells responding to the same activation with continuous firing. IT was evoked by depolarizing voltage ramps exceeding 46 mV/s and increased with ramp slope (240–2,400 mV/s). Bath application of 200 μM Ni2+ depressed ramp-activated IT. Phasic firing recorded in current clamp could only be activated by membrane depolarizations exceeding ∼43–46 mV/s and was blocked by Ni2+ and mibefradil, suggesting IT as an underlying mechanism. Two components of IT, “fast” and “slow,” were isolated based on a difference in time constant of inactivation (12 ms and 177 ms, respectively). The amplitude of the fast subtype depended on the slope of membrane depolarization and was twice as great in burst-firing cells than in cells having a tonic discharge. Post hoc single-cell RT-PCR analyses suggested that the fast component is associated with the CaV3.1 channel subtype. IT may enhance responses of phasic-firing dorsal horn neurons to rapid membrane depolarizations and contribute to an ability to discriminate between afferent sensory inputs that encode high- and low-frequency stimulus information.


1989 ◽  
Vol 61 (3) ◽  
pp. 467-477 ◽  
Author(s):  
D. E. Meyers ◽  
J. L. Barker

1. Voltage-dependent calcium currents in embryonic (E18) hippocampal neurons cultured for 1-14 days were investigated using the whole-cell patch-clamp technique. 2. Calcium currents were isolated by removing K+ from both the internal and external solutions. In most recordings the external solution contained tetrodotoxin, tetraethylammonium ions, and low concentrations of Na+, whereas the internal solution contained the large cations and anions, N-methyl-D-glucamine and methanesulphonate, and an adenosine 5'-triphosphate (ATP) regenerating system (Forscher and Oxford, 1985) to retard “run-down” of Ca currents. 3. Under these conditions, the sustained inward current triggered during depolarizing steps was enhanced when extracellular [Ca2+] ([Ca2+]0) was raised from 2 to 10 mM and abolished when [Ca2+]0 was lowered to 0.1 mM or by addition of Co2+ ions. These results indicate that the inward current was carried primarily by Ca2+ ions and was designated ICa. This current may be comparable to the “high-voltage-activated” Ca current described in other preparations. 4. In cells cultured for 1-3 days, ICa was small or absent (less than 20 pA for cells 1 day in culture and less than 80 pA for cells 3 days in culture). Although ICa decayed considerably during depolarizing steps, there was little evidence of the transient calcium current (T current) that was recorded in approximately 40% of cells cultured longer than 6 days. Maximal (i.e., the largest) ICa increased from 20 to 80 pA in 1- to 3-day cells to 150–450 pA in cells cultured for longer than 6 days. 5. The decay of ICa elicited by depolarizations from holding potentials of -60 mV or more negative was usually greatest for the maximal ICa. Replacement of extracellular Ca2+ (4 mM) with Ba2+ (2 mM) resulted in a substantial decrease in the extent of decay of ICa and a shift of the I-V relation in the hyperpolarizing direction. 6. Qualitative data obtained from experiments in which different levels of internal Ca2+ buffering were employed demonstrated that, on average, the decay of ICa was reduced as the capacity and/or rate of buffering was increased. The mean decay of ICa in cells buffered with 5 mM 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) was 9 +/- 7 (SD) %, (n = 12) and 25 +/- 12%, (n = 12) for cells buffered with the same concentration of ethyleneglycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA).(ABSTRACT TRUNCATED AT 400 WORDS)


1991 ◽  
Vol 260 (3) ◽  
pp. H735-H743 ◽  
Author(s):  
B. Fermini ◽  
R. D. Nathan

The whole cell configuration of the patch-clamp technique was used to test the hypothesis that the presence of sialic acid residues influences both T- and L-type Ca2+ currents (ICa,T and ICa,L) in cultured pacemaker cells isolated from the rabbit sinoatrial node. Removal of these anionic sugar moieties by neuraminidase (1.0 U/ml for 5-20 min) increased ICa,T in five of nine cells (by a factor of 2.2-5.1) and ICa,L in three of six cells (by a factor of 1.2-1.6). In cells that did not exhibit such an increase, the enzyme reduced ICa,T but had no significant effect on ICa,L. In cells that exhibited an increase in ICa,T, exposure to neuraminidase also shifted the activation curve to more negative potentials and increased the slope of the inactivation curve. The enzyme did not influence the gating of ICa,L or the rates of inactivation of either ICa,T or ICa,L. The enhancement of ICa,T and ICa,L could not be mimicked by including neuraminidase in the patch pipette or by adding a contaminant of the enzyme preparation, phospholipase C, to the bath. When external Ca2+ was replaced by Ba2+, neither ICa,T nor ICa,L was increased significantly by neuraminidase. It is proposed that by removing sialic acid residues neuraminidase might directly alter the gating of T-type Ca2+ channels. On the other hand, the increased amplitudes of ICa,T and ICa,L might be due to a rise in intracellular Ca2+.


2017 ◽  
Vol 40 (2) ◽  
pp. 264-276 ◽  
Author(s):  
Xiaoli Yang ◽  
Gang Dong ◽  
K. Palaniappan ◽  
Guohua Mi ◽  
Tobias I. Baskin

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