Generation of action potentials in Chara corallina by turgor pressure changes

Planta ◽  
1978 ◽  
Vol 138 (2) ◽  
pp. 173-179 ◽  
Author(s):  
Ulrich Zimmermann ◽  
Friedrich Beckers
2009 ◽  
Vol 36 (5) ◽  
pp. 383 ◽  
Author(s):  
John S. Boyer

Recently discovered reactions allow the green alga Chara corallina (Klien ex. Willd., em. R.D.W.) to grow well without the benefit of xyloglucan or rhamnogalactan II in its cell wall. Growth rates are controlled by polygalacturonic acid (pectate) bound with calcium in the primary wall, and the reactions remove calcium from these bonds when new pectate is supplied. The removal appears to occur preferentially in bonds distorted by wall tension produced by the turgor pressure (P). The loss of calcium accelerates irreversible wall extension if P is above a critical level. The new pectate (now calcium pectate) then binds to the wall and decelerates wall extension, depositing new wall material on and within the old wall. Together, these reactions create a non-enzymatic but stoichiometric link between wall growth and wall deposition. In green plants, pectate is one of the most conserved components of the primary wall, and it is therefore proposed that the acceleration-deceleration-wall deposition reactions are of wide occurrence likely to underlie growth in virtually all green plants. C. corallina is one of the closest relatives of the progenitors of terrestrial plants, and this review focuses on the pectate reactions and how they may fit existing theories of plant growth.


1981 ◽  
Vol 68 (3) ◽  
pp. 553-559 ◽  
Author(s):  
William J. Lucas ◽  
Jon M. Alexander

2006 ◽  
Vol 98 (1) ◽  
pp. 93-105 ◽  
Author(s):  
TIMOTHY E. PROSEUS ◽  
JOHN S. BOYER

2017 ◽  
Vol 89 (2) ◽  
pp. 69-72
Author(s):  
Piotr Wałęga ◽  
Michał Romaniszyn ◽  
Maciej Wałęga ◽  
Jarosław Szymon Świrta ◽  
Wojciech Nowak

Aim: The aim of this study was to present our preliminary experience with intraoperative neuromonitoring during rectal resection. Materials and methods: We qualified 4 patients (2 women, 2 men; age 42 – 53 years) with rectal cancer for surgery with intraoperative neuromonitoring. In all patients, functional tests of the anorectal area were performed before surgery. Action potentials from the sphincter complex in response to nerve fiber stimulation were recorded with electrodes implanted before surgery. Moreover, we inserted a standard, 18FR Foley’s urinary catheter to which a T-tube was connected to allow urine outflow and measurement of pressure changes in the bladder induced by detrusor contractions during stimulation. Results: Setting up neuromonitoring prolonged surgery time by 30 to 40 minutes, or even by 60 to 80 minutes in the case of the first two patients. Neuromonitoring itself took additional 20 to 30 minutes during surgery. In all patients, we stimulated branches of the inferior hypogastric plexus in their anatomical position during dissection. In three patients, we evoked responses both from the bladder and the sphincter in all planes of stimulation. In one patient, there was no response from the left side of the bladder, and in the same patient, we observed symptoms of neurogenic bladder. Conclusions: Based on the available literature and our own experience, we state that monitoring of bladder pressure and electromyographic signals from rectal sphincters enables visualization and preservation of autonomic nervous system structures, both sympathetic and parasympathetic. Intraoperative signals seem to be correlated with clinical presentation and functional examinations after surgery. In order to objectify our results, it is necessary to perform functional examinations before and after surgery in a larger group of patients.


2001 ◽  
Vol 28 (7) ◽  
pp. 551 ◽  
Author(s):  
Virginia A. Shepherd ◽  
Teruo Shimmen ◽  
Mary J. Beilby

Chara cells produce receptor potentials (RPDs) in response to mechanical stimulation. We have used a mechanostimulatory device to compare characteristics of touch-activated RPDs and action potentials (APs) when cell turgor pressure was changed. The device delivered a series of mechanical stimulations of increasing energy (F0.5, F1, F2, F3, F4, F5 and F6). Cells were alternately stimulated in artificial pondwater (APW) and a sorbitol series, in long-term experiments, involving up to six solution changes. The calculated cell turgor pressures were about 0.6 MPa (APW), and 0.49 MPa, 0.37 MPa, 0.24 MPa and 0.12 MPa in 50, 100, 150 and 200 mM sorbitol–APW, respectively. In other experiments, cells were pre-conditioned in the sorbitol solutions, and then transferred to APW. All cells were allowed long recovery periods (40–60 min) after APs or solution transfers. Only small changes in cell conductance were observed in I–V and G–V analysis of unstimulated cells after reducing turgor pressure from 0.59 MPa to 0.24 MPa. In APW, the RPDs increased in amplitude and duration with increased stimulus energy until the threshold RPD was reached, and an AP was triggered, usually between stimulus F4 and F5. Cells with decreased turgor pressure became more sensitive to stimulation, giving threshold RPDs or APs with smaller stimulus (e.g. between F0.5 and F3). Conversely, an increase in cell turgor pressure (return to APW) led to a decrease in sensitivity to stimulus. When turgor pressure was greatly decreased (to 0.12 MPa), some cells became unresponsive or gave unusual responses. However, only the mechanical part of the touch response was affected by changing the cell turgor pressure. The mean amplitudes of the subthreshold and threshold RPD (that triggers the AP), and of the touch-activated APs, were independent of cell turgor pressure, although action potentials had smaller amplitude when turgor was reduced to about 0.12 MPa. The amplitude of the subthreshold RPD was close to 20 mV, and the amplitude of the threshold RPD was close to 50 mV, in all cells. If tension of the cell wall–plasma membrane–cytoskeleton complex decreased along with decreased cell turgor pressure, a given stimulus could stretch the complex to a greater extent, resulting in activation of more mechanosensory channels. The effect on the RPD of changes in cell turgor pressure is discussed in relation to the mechanical properties of the cell wall–plasma membrane–cytoskeleton complex.


2005 ◽  
Vol 95 (6) ◽  
pp. 967-979 ◽  
Author(s):  
TIMOTHY E. PROSEUS ◽  
JOHN S. BOYER

1955 ◽  
Vol 180 (2) ◽  
pp. 261-276 ◽  
Author(s):  
William Sleator ◽  
Harvey R. Butcher

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