scholarly journals BIOELECTRIC POTENTIALS IN HALICYSTIS

1940 ◽  
Vol 23 (4) ◽  
pp. 495-520 ◽  
Author(s):  
L. R. Blinks

The effects of light upon the potential difference across the protoplasm of impaled Halicystis cells are described. These effects are very slight upon the normal P.D., increasing it 3 or 4 per cent, or at most 10 per cent, with a characteristic cusped time course, and a corresponding decrease on darkening. Light effects become much greater when the P.D. has been decreased by low O2 content of the sea water; light restores the P.D. in much the same time course as aeration, and doubtless acts by the photosynthetic production of O2. There are in both cases anomalous cusps which decrease the P.D. before it rises. Short light exposures may give only this anomaly. Over part of the potential range the light effects are dependent upon intensity. Increased CO2 content of the sea water likewise depresses the P.D. in the dark, and light overcomes this depression if it is not carried too far. Recovery is probably due to photosynthetic consumption of CO2, unless there is too much present. Again there are anomalous cusps during the first moments of illumination, and these may be the only effect if the P.D. is too low. The presence of ammonium salts in the sea water markedly sensitizes the cells to light. Subthreshold NH4 concentrations in the dark become effective in the light, and the P.D. reverses to a negative sign on illumination, recovering again in the dark. This is due to increase of pH outside the cell as CO2 is photosynthetically reduced, with increase of undissociated NH3 which penetrates the cell. Anomalous cusps which first carry the P.D. in the opposite direction to the later drift are very marked in the presence of ammonia, and may represent an increased acidity which precedes the alkaline drift of photosynthesis. This acid gush seems to be primarily within the protoplasm, persisting when the sea water is buffered. Glass electrode measurements also indicate anomalies in the pH drift. There are contrary cusps on darkening which suggest temporarily increased alkalinity. Even more complex time courses are given by combining low O2 and NH4 exposures with light; these may have three or more cusps, with reversal, recovery, and new reversal. The ultimate cause of the light effects is to be found in an alteration of the surface properties by the treatments, which is overcome (low O2, high CO2), or aided (NH4) by light. This alteration causes the surface to lose much of its ionic discrimination, and increases its electrical resistance. Tests with various anion substitutions indicate this, with recovery of normal response in the light. A theory of the P.D. in Halicystis is proposed, based on low mobility of the organic anions of the protoplasm, with differences in the two surfaces with respect to these, and the more mobile Na and K. ions.

1942 ◽  
Vol 25 (6) ◽  
pp. 905-916 ◽  
Author(s):  
L. R. Blinks

The effect of temperature upon the bioelectric potential across the protoplasm of impaled Valonia cells is described. Over the ordinary tolerated range, the P.D. is lowest around 25°C., rising both toward 15° and 35°. The time curves are characteristic also. The magnitude of the temperature effect can be controlled by changing the KCl content of the sea water (normally 0.012 M): the magnitude is greatly reduced at 0.006 M KCl, enhanced at 0.024 M, and greatly exaggerated at 0.1 M KCl. Conversely, temperature controls the magnitude of the potassium effect, which is smallest at 25°, with a cusped time course. It is increased, with a smoothly rising course, at 15°, and considerably enhanced, with only a small cusp, at 35°. A temporary "alteration" of the protoplasmic surface by the potassium is suggested to account for the time courses. This alteration does not occur at 15°; the protoplasm recovers only slowly and incompletely at 25°, but rapidly at 35°, in such fashion as to make the P.D. more negative than at 15°. This would account for the temperature effects observed in ordinary sea water.


1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.


1989 ◽  
Vol 62 (6) ◽  
pp. 1280-1286 ◽  
Author(s):  
N. Uchimura ◽  
E. Cherubini ◽  
R. A. North

1. Intracellular recordings were made from neurons in slices cut from the rat nucleus accumbens septi. Membrane currents were measured with a single-electrode voltage-clamp amplifier in the potential range -50 to -140 mV. 2. In control conditions (2.5 mM potassium), the resting membrane potential of the neurons was -83.4 +/- 1.1 (SE) mV (n = 157). Steady state membrane conductance was voltage dependent, being 34.8 +/- 1.7 nS (n = 25) at -100 mV and 8.0 +/- 0.7 nS (n = 25) at -60 mV. 3. Barium (1 microM) markedly reduced the inward rectification and caused a small inward current (40.6 +/- 8.7 pA, n = 8) at the resting potential. These effects became larger with higher barium concentrations, and, in 100 microM barium, the current-voltage relation was straight. 4. The block of the inward current by barium (at -130 mV) occurred with an exponential time course; the time constant was approximately 1 s at 1 microM barium and less than 90 ms with 100 microM. Strontium had effects similar to those of barium, but 1000-fold higher concentrations were required. Cesium chloride (2 mM) and rubidium chloride (2 mM) also blocked the inward rectification; their action reached steady state within 50 ms. 5. It is concluded that the nucleus accumbens neurons have a potassium conductance with many features of a typical inward rectifier and that this contributes to the potassium conductance at the resting potential.


1991 ◽  
Vol 97 (2) ◽  
pp. 303-320 ◽  
Author(s):  
A Castellano ◽  
J López-Barneo

Voltage-gated Na+ and Ca2+ conductances of freshly dissociated septal neurons were studied in the whole-cell configuration of the patch-clamp technique. All cells exhibited a large Na+ current with characteristic fast activation and inactivation time courses. Half-time to peak current at -20 mV was 0.44 +/- 0.18 ms and maximal activation of Na+ conductance occurred at 0 mV or more positive membrane potentials. The average value was 91 +/- 32 nS (approximately 11 mS cm-2). At all membrane voltages inactivation was well fitted by a single exponential that had a time constant of 0.44 +/- 0.09 ms at 0 mV. Recovery from inactivation was complete in approximately 900 ms at -80 mV but in only 50 ms at -120 mV. The decay of Na+ tail currents had a single time constant that at -80 mV was faster than 100 microseconds. Depolarization of septal neurons also elicited a Ca2+ current that peaked in approximately 6-8 ms. Maximal peak Ca2+ current was obtained at 20 mV, and with 10 mM external Ca2+ the amplitude was 0.35 +/- 0.22 nA. During a maintained depolarization this current partially inactivated in the course of 200-300 ms. The Ca2+ current was due to the activity of two types of conductances with different deactivation kinetics. At -80 mV the closing time constants of slow (SD) and fast (FD) deactivating channels were, respectively, 1.99 +/- 0.2 and 0.11 +/- 0.03 ms (25 degrees C). The two kinds of channels also differed in their activation voltage, inactivation time course, slope of the conductance-voltage curve, and resistance to intracellular dialysis. The proportion of SD and FD channels varied from cell to cell, which may explain the differential electrophysiological responses of intracellularly recorded septal neurons.


1980 ◽  
Vol 152 (5) ◽  
pp. 1302-1310 ◽  
Author(s):  
D S Pisetsky ◽  
G A McCarty ◽  
D V Peters

The quantitative expression of anti-DNA and anti-Sm antibodies has been investigated in autoimmune MRL-lpr/lpr and MRL-+/+ mice. Anti-Sm antibodies were detected in sera from 21/23 lpr/lpr and 10/16 +/+ mice, with individual animals showing striking variation in the time-course and magnitude of this autoantibody response. The peak antibody levels of the responding animals of each substrain did not differ significantly. For anti-DNA antibody, a different pattern of responsiveness was observed. Individual animals of each substrain produced very similar responses in terms of the magnitude and time-course of serum anti-DNA antibody. The differences in the peak levels of the two substrains were highly significant, with lpr/lpr mice demonstrating a much greater anti-DNA antibody response than +/+ mice. In lpr/lpr mice tested for both autoantibody systems, serum anti-DNA and anti-Sm antibodies showed distinct time-courses. These studies indicate that anti-DNA and anti-Sm antibodies are expressed independently in MRL mice, with the expression of anti-DNA, but not anti-Sm antibody markedly influenced by the presence of the 1pr gene. A fundamental difference in the mechanisms involved in the generation of anti-DNA and anti-Sm antibodies is suggested by the quantitative pattern of the two responses.


1939 ◽  
Vol 23 (1) ◽  
pp. 53-57 ◽  
Author(s):  
W. J. V. Osterhout

Interest in the study of Halicystis and of Valonia has been stimulated by discoveries of marked contrasts and striking similarities existing side by side. This is illustrated by new experiments with the alkali metals and alkaline earths. In Halicystis the apparent mobilities of K+, Rb+, Cs+, and Li+ (calculated by means of Henderson's equation from changes in P.D. produced by replacing sea water by a mixture of equal parts of sea water and 0.6 M of various chlorides) are as follows, uK, = 16, uRb = 16, uCs = 4.4, and uLi = 0.2; uNa is taken as 0.2. These values resemble those in Valonia except that in the latter uCs is about 0.2. No calculation is made for uNHNH4, because in these experiments even at low pH so much NH3 is present that the sign of the P.D. may reverse. This does not happen with Valonia. According to Blinks, NH4+ at pH 5 in low concentrations acts like K+. The calculation gives uMg = 1.9 which is similar to the value found for Valonia. No calculation can be made for CaCl2 since it produces protoplasmic alterations and in consequence Henderson's equation does not apply. This differs from Valonia. Evidently these plants agree closely in some aspects of electrical behavior but differ widely in others.


2015 ◽  
Vol 146 (1) ◽  
pp. 15-36 ◽  
Author(s):  
Giovanni Gonzalez-Gutierrez ◽  
Claudio Grosman

The superfamily of pentameric ligand-gated ion channels (pLGICs) is unique among ionotropic receptors in that the same overall structure has evolved to generate multiple members with different combinations of agonist specificities and permeant-ion charge selectivities. However, aside from these differences, pLGICs have been typically regarded as having several invariant functional properties. These include pore blockade by extracellular quaternary-ammonium cations in the micromolar-to-millimolar concentration range (in the case of the cation-selective members), and a gain-of-function phenotype, which manifests as a slower deactivation time course, as a result of mutations that reduce the hydrophobicity of the transmembrane pore lining. Here, we tested this notion on three distantly related cation-selective members of the pLGIC superfamily: the mouse muscle nicotinic acetylcholine receptor (nAChR), and the bacterial GLIC and ELIC channels. Remarkably, we found that, whereas low millimolar concentrations of TMA+ and TEA+ block the nAChR and GLIC, neither of these two quaternary-ammonium cations blocks ELIC at such concentrations; instead, both carry measurable inward currents when present as the only cations on the extracellular side. Also, we found that, whereas lidocaine binding speeds up the current-decay time courses of the nAChR and GLIC in the presence of saturating concentrations of agonists, the binding of lidocaine to ELIC slows this time course down. Furthermore, whereas mutations that reduce the hydrophobicity of the side chains at position 9′ of the M2 α-helices greatly slowed the deactivation time course of the nAChR and GLIC, these mutations had little effect—or even sped up deactivation—when engineered in ELIC. Our data indicate that caution should be exercised when generalizing results obtained with ELIC to the rest of the pLGICs, but more intriguingly, they hint at the possibility that ELIC is a representative of a novel branch of the superfamily with markedly divergent pore properties despite a well-conserved three-dimensional architecture.


2014 ◽  
Vol 5 ◽  
pp. JCM.S13738 ◽  
Author(s):  
Satoru Sakuma ◽  
Daisuke Tokuhara ◽  
Hiroshi Otsubo ◽  
Tsunekazu Yamano ◽  
Haruo Shintaku

Background The time course of cytokine dynamics after seizure remains controversial. Here we evaluated the changes in the levels and sites of interleukin (IL)-1β expression over time in the hippocampus after seizure. Methods Status epilepticus (SE) was induced in adult Wistar rats by means of intraperitoneal injection of kainic acid (KA). Subsequently, the time courses of cellular localization and IL-1β concentration in the hippocampus were evaluated by means of immunohistochemical and quantitative assays. Results On day 1 after SE, CA3 pyramidal cells showed degeneration and increased IL-1β expression. In the chronic phase (>7 days after SE), glial fibrillary acidic protein (GFAP)–-positive reactive astrocytes–-appeared in CA1 and became IL-1β immunoreactive. Their IL-1β immunoreactivity increased in proportion to the progressive hypertrophy of astrocytes that led to gliosis. Quantitative analysis showed that hippocampal IL-1β concentration progressively increased during the acute and chronic phases. Conclusion IL-1β affects the hippocampus after SE. In the acute phase, the main cells expressing IL-1β were CA3 pyramidal cells. In the chronic phase, the main cells expressing IL-1β were reactive astrocytes in CA1.


2012 ◽  
Vol 7 ◽  
Author(s):  
Roberto W. Dal Negro ◽  
Silvia Tognella ◽  
Luca Bonadiman ◽  
Paola Turco

Background: Information on the effects of long-term oxygen treatment (LTOT) on blood hemoglobin (Hb) in severe COPD are limited. The aim was to assess blood Hb values in severe COPD, and investigate the time-course of both Hb and blood gas changes during a 3-year telemetric LTOT. Methods: A cohort of 132 severe COPD patients (94 males; 71.4 years ± 8.8 sd), newly admitted to the tele-LTOT program, was investigated. Subjects were divided according to their original blood Hb: group A: <13 g/dL; group B: ≥13<15 g/dL; group C: ≥ 5<16 g/dL; group D: ≥16 g/dL. Blood Hb (g/dL), PaO2 and PaCO2 (mmHg), SaO2 (%), and BMI were measured at LTOT admission (t0), and at least quarterly over three years (t1-t3). Wilcoxon test was used to compare t0 vs. t1 values; linear regression to assess a possible Hb-BMI relationship; ANOVA to compare changes in Hb time-courses over the 3 years. Results: LTOT induced a systematic increase of PaO2, and changes were significant since the first year (from 52.1 mmHg± 6.6sd to 65.1 mmHg± 8.7 sd, p<0.001). Changes in SaO2 were quite similar. Comparable and equally significant trends were seen in all subgroups (p<0.001). PaCO2 dropped within the first year of LTOT (from 49.4 mmHg± 9.1sd to 45.9 mmHg ±7.5 sd, p<0.001): the t0-t1 comparison proved significant (p<0.01) only in subgroups with the highest basal Hb, who showed a further PaCO2 decline over the remaining two years (p<0.001). Hb tended to normalization during LTOT only in subgroups with basal Hb>15 g/dl (ANOVA p<0.001); anemic subjects (Hb<13 g/dl) ameliorated not significantly in the same period (ANOVA = 0.5). Survival was independent of the original blood Hb. Anemia and polyglobulia are differently prevalent in COPD, the latter being the most represented in our cohort. LTOT affected both conditions, but to a different extent and according to different time-courses. The most striking Hb improvement was in polyglobulic patients in whom also PaO2, PaCO2 and SaO2 dramatically improved. In anemic subjects effects were smaller and slower, oxygenation being equally ameliorated by LTOT. Conclusions: LTOT effects on Hb and PaCO2 are regulated by an Hb-dependent gradient which seems independent of the original impairment of blood gases and of effects on oxygenation.


1988 ◽  
Vol 138 (1) ◽  
pp. 1-15 ◽  
Author(s):  
P. TYTLER ◽  
J. H. BLAXTER

Drinking responses to salinity change in the larvae of herring (Clupea harengus L.), plaice (Pleuronectes platessa L.) and cod (Gadus morhua L.) were measured from the time course of uptake of dextran labelled with tritium, following immersion in solutions of 32‰ and 16‰ sea water. The yolk sac and first feeding larval stages of all three species drink in both salinities. Furthermore, post-yolk sac stages appear to adjust their drinking rates to compensate for different salinities in a manner similar to that of the adults. Drinking rates in 32‰ sea water are approximately double those in 16‰. Mass-related drinking rates of larvae are higher than those in adults, but the differences do not match the differences in surface area to mass ratios, suggesting that larval skin is less permeable to water than is adult gill epithelium. Water absorption is indicated by the evidence of concentration of dextran in the gut. The estimates of drinking rates from tritiated dextran uptake are supported by epifluorescence microscopical measurements of the uptake of fluorescein isothiocyanate dextran.


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