scholarly journals An Electrophysiological Study of Neuroglandular Transmission in the Isolated Salivary Glands of the Cockroach

1973 ◽  
Vol 58 (1) ◽  
pp. 29-43
Author(s):  
C. R. HOUSE
Keyword(s):  
Membrane Potential ◽  
Salivary Glands ◽  
Gland Cell ◽  
Electrical Response ◽  
Electrophysiological Study ◽  
Ringer Solution ◽  
Nervous Stimulation ◽  
External Potassium ◽  
Increase Membrane Permeability ◽  
Initial Latency

1. Some aspects of neuroglandular transmission in isolated salivary glands of the cockroach have been studied. 2. The membrane potential of acinar cells is -32.3±0.8 mV (mean±S..E; N = 600 cells) when the gland is bathed in Ringer solution. 3. Upon delivering a single shock by ‘field stimulation’ to the salivary nerves the gland cell membrane undergoes after an initial latency of 1 second a transient hyperpolarization of about 1-30 mV which lasts for about 10 sec. 4. When the salivary nerves are stimulated by trains of current pulses the hyperpolarization that occurs is larger in amplitude and longer in duration than that after a single stimulus. 5. The amplitude of the responses to single shocks and stimulus trains depends on the external potassium concentration. Thus, the neurotransmitter may increase membrane permeability to potassium ions. 6. The electrical response of the gland cell to 5-hydroxytryptamine in concentrations from 2.5-250x10-7 M is similar in sign and magnitude to that of nervous stimulation. 7. Occasionally small fluctuations in the membrane potential are observed and these are similar in sign and duration to responses elicited by single shocks to the salivary nerves.

Stimulus-secretion coupling in an insect salivary gland: cell activation by elevated potassium concentrations

1975 ◽  
Vol 62 (3) ◽  
pp. 629-636
Author(s):  
M. J. Berridge ◽  
B. D. Lindley ◽  
W. T. Prince
Keyword(s):  
Salivary Glands ◽  
Cell Activation ◽  
Gland Cell ◽  
Fluid Secretion ◽  
Salivary Gland Cell ◽  
Primary Role ◽  
High Potassium ◽  
External Potassium ◽  
Stimulus Secretion Coupling ◽  
External Calcium

1. Fluid secretion by isolated salivary glands was stimulated by elevating the external potassium concentration. 2. The stimulatory effect of potassium was dependent on external calcium and was potentiated by a subthreshold dose of 5-hydroxytryptamine (5-HT). 3. During the action of 120 mM potassium there was a large calciumdependent decrease in transepithelial resistance similar to that produced with 5-HT at normal potassium concentrations. 4. These results on Calliphora salivary glands are compared with other cases where cells are activated by high potassium. In most cases, the effect of high potassium is dependent upon calcium, suggesting that the latter plays a primary role in cell activation.

Studies on the mechanism of fluid secretion by isolated salivary glands of Calliphora

1976 ◽  
Vol 64 (2) ◽  
pp. 311-322
Author(s):  
M. J. Berridge ◽  
B. D. Lindley ◽  
W. T. Prince
Keyword(s):  
Salivary Glands ◽  
Apical Membrane ◽  
Potassium Concentration ◽  
Basal Membrane ◽  
Fluid Secretion ◽  
Sodium Permeability ◽  
Bathing Medium ◽  
Major Cation ◽  
Diuretic Agent ◽  
External Potassium

1. Potassium is the major cation in the secretion of the salivary glands of Calliphora and is necessary for full secretory rates. 2. Other ions (rubidium and sodium) can support secretion in the absence of potassium. 39. During stimulation with 5-HT a Nernst plot of the basal membrane potential has a slope of 53 mV for a tenfold change in external potassium concentration and the slope at rest deviates from this over the range I-20 mM external potassium. 4. Hyperpolarization of the basal membrane by 5-HT is abolished if the chloride in the bathing medium is replaced by isethionate. 5. The diuretic agent amiloride inhibits fluid secretion by a mechanism which may include a reduction in calcium entry in addition to its recognized effect on sodium permeability. 6. A model is proposed in which fluid secretion is driven by the active transport of potassium across the apical membrane with chloride following passively.

scholarly journals Relationships between resting conductances, excitability, and t-system ionic homeostasis in skeletal muscle

2011 ◽  
Vol 138 (1) ◽  
pp. 95-116 ◽  
Author(s):  
James A. Fraser ◽  
Christopher L.-H. Huang ◽  
Thomas H. Pedersen
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Conduction Velocity ◽  
Electrical Response ◽  
Quantitative Description ◽  
Ion Concentration ◽  
Ionic Homeostasis ◽  
Voltage Gated ◽  
Concentration Changes ◽  
T System

Activation of skeletal muscle fibers requires rapid sarcolemmal action potential (AP) conduction to ensure uniform excitation along the fiber length, as well as successful tubular excitation to initiate excitation–contraction coupling. In our companion paper in this issue, Pedersen et al. (2011. J. Gen. Physiol. doi:10.1085/jgp.201010510) quantify, for subthreshold stimuli, the influence upon both surface conduction velocity and tubular (t)-system excitation of the large changes in resting membrane conductance (GM) that occur during repetitive AP firing. The present work extends the analysis by developing a multi-compartment modification of the charge–difference model of Fraser and Huang to provide a quantitative description of the conduction velocity of actively propagated APs; the influence of voltage-gated ion channels within the t-system; the influence of t-system APs on ionic homeostasis within the t-system; the influence of t-system ion concentration changes on membrane potentials; and the influence of Phase I and Phase II GM changes on these relationships. Passive conduction properties of the novel model agreed with established linear circuit analysis and previous experimental results, while key simulations of AP firing were tested against focused experimental microelectrode measurements of membrane potential. This study thereby first quantified the effects of the t-system luminal resistance and voltage-gated Na+ channel density on surface AP propagation and the resultant electrical response of the t-system. Second, it demonstrated the influence of GM changes during repetitive AP firing upon surface and t-system excitability. Third, it showed that significant K+ accumulation occurs within the t-system during repetitive AP firing and produces a baseline depolarization of the surface membrane potential. Finally, it indicated that GM changes during repetitive AP firing significantly influence both t-system K+ accumulation and its influence on the resting membrane potential. Thus, the present study emerges with a quantitative description of the changes in membrane potential, excitability, and t-system ionic homeostasis that occur during repetitive AP firing in skeletal muscle.

Depolarization modulates endothelial cell calcium influx and microvessel permeability

1991 ◽  
Vol 261 (4) ◽  
pp. H1246-H1254 ◽  
Author(s):  
P. He ◽  
F. E. Curry
Keyword(s):  
Membrane Potential ◽  
Calcium Concentration ◽  
Calcium Influx ◽  
Ringer Solution ◽  
Initial Increase ◽  
High Potassium ◽  
Microvessel Permeability ◽  
Microvessel Wall ◽  
Initial Peak ◽  
Peak Value

We investigated the mechanisms whereby high-potassium (57.9 mM) Ringer solutions attenuate the increase in permeability caused when microvessels are exposed to the calcium ionophores ionomycin and A23187 (5 microM). In single perfused microvessels we measured cytoplasmic calcium concentration, [Ca2+]i, in the cells forming the microvessel wall and the hydraulic conductivity, Lp, to follow changes in the permeability of the microvessel walls. In normal Ringer solution, [Ca2+]i was increased to an initial peak value of 226 +/- 12 nM after exposure to calcium ionophores; the corresponding increase in microvessel Lp was 10.3 +/- 2.6 times control. With high-potassium solutions, the peak value of [Ca2+]i was 133 +/- 12 nM and Lp was increased to only 2.5 +/- 0.7 times control. Increasing extracellular calcium from 1.1 to 5 mM with high potassium restored the initial peak value of [Ca2+]i to 303 +/- 38 nM. The increases in both [Ca2+]i and Lp were abolished in calcium-free solutions. If high-potassium solutions depolarize the cells forming the microvessel wall as indicated by the membrane potential-sensitive dye bisoxonol, then the magnitude of the initial increase in [Ca2+]i could be accounted for by changes in the electrochemical driving force through conductive channels for calcium ion. Our results conform to the hypothesis that the permeability properties of microvessels are modulated by changes in the membrane potential of the endothelial cells and/or pericytes forming the microvessel wall.

scholarly journals Relative Ion Permeabilities in the Crayfish Giant Axon Determined from Rapid External Ion Changes

1967 ◽  
Vol 50 (7) ◽  
pp. 1929-1953 ◽  
Author(s):  
Alfred Strickholm ◽  
B. Gunnar Wallin
Keyword(s):  
Membrane Potential ◽  
Potassium Level ◽  
Potassium Concentration ◽  
Giant Axon ◽  
Resting Potential ◽  
Resting Membrane Potential ◽  
Constant Field ◽  
Appreciable Effect ◽  
Ion Concentrations ◽  
External Potassium

The changes in membrane potential of isolated, single crayfish giant axons following rapid shifts in external ion concentrations have been studied. At normal resting potential the immediate change in membrane potential after a variation in external potassium concentration is quite marked compared to the effect of an equivalent chloride change. If the membrane is depolarized by a maintained potassium elevation, the immediate potential change due to a chloride variation becomes comparable to that of an equivalent potassium change. There is no appreciable effect on membrane potential when external sodium is varied, at normal or at a depolarized membrane potential. Starting from the constant field equation, expressions for the permeability ratios PCl/PK, PNa/PK, and for intracellular potassium and chloride concentrations are derived. At normal resting membrane potential, PCl/PK is 0.13 but at a membrane potential of -53 mv (external potassium level increased about five times) it is 0.85. The intracellular concentrations of potassium and chloride are estimated to be 233 and 34 mM, respectively, and it is pointed out that this is not compatible with ions distributed in a Nernst equilibrium across the membrane. It is also stressed that the information given by a plot of membrane potential vs. the logarithm of external potassium concentrations is very limited and rests upon several important assumptions.

Responsiveness to D-glucose in neurosecretory cells of crustaceans

1993 ◽  
Vol 70 (2) ◽  
pp. 758-764 ◽  
Author(s):  
E. Garcia ◽  
A. Benitez ◽  
C. G. Onetti
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Electrophysiological Study ◽  
Reversal Potential ◽  
Neurosecretory Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Long Time ◽  
Glucose Sensitivity ◽  
Discharge Patterns

1. An electrophysiological study of the D-glucose sensitivity of X-organ (XO) neurosecretory cell bodies in crayfish was carried out with the use of microelectrodes, perforated, and cell-attached patch-clamp techniques. 2. Glucose depolarizes the membrane potential of XO cells in a concentration-dependent manner. 3. Depolarization produced by glucose initiates a change in the pattern of electrical activity. Silent cells began to discharge action potentials. When bursting cells are depolarized by glucose, their action potentials are no longer grouped in bursts or disappear entirely. 4. Although the membrane potential returns to its initial value after removing glucose from the bath, discharge patterns of the cells may remain different. This suggests that besides the depolarizing effect, once the cells have been exposed to glucose, the sugar switches on a process that is maintained for a long time. 5. Glucose produced a reduction of membrane steady-state conductance, and a shift of reversal potential of membrane currents to a more positive value. 6. Depolarization induced by D-glucose appears to be related with a closure of potassium channels. 7. Glucose effect was thought to be generated by a product of metabolism that would act as intracellular mediator.

scholarly journals The Influence of External Potassium on the Inactivation of Sodium Currents in the Giant Axon of the Squid, Loligo pealei

1969 ◽  
Vol 53 (6) ◽  
pp. 685-703 ◽  
Author(s):  
William J. Adelman ◽  
Yoram Palti
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Membrane Conductance ◽  
Absolute Magnitude ◽  
Giant Axon ◽  
Membrane Potentials ◽  
Initial Transient ◽  
External Potassium ◽  
Loligo Pealei ◽  
External K

Isolated giant axons were voltage-clamped in seawater solutions having constant sodium concentrations of 230 mM and variable potassium concentrations of from zero to 210 mM. The inactivation of the initial transient membrane current normally carried by Na+ was studied by measuring the Hodgkin-Huxley h parameter as a function of time. It was found that h reaches a steady-state value within 30 msec in all solutions. The values of h∞, τh, αh,and ßh as functions of membrane potential were determined for various [Ko]. The steady-state values of the h parameter were found to be inversely related, while the time constant, τh, was directly related to external K+ concentration. While the absolute magnitude as well as the slopes of the h∞ vs. membrane potential curves were altered by varying external K+, only the magnitude and not the shape of the corresponding τh curves was altered. Values of the two rate constants, αh and ßh, were calculated from h∞ and τh values. αh is inversely related to [Ko] while ßh is directly related to [Ko] for hyperpolarizing membrane potentials and is independent of [Ko] for depolarizing membrane potentials. Hodgkin-Huxley equations relating αh and ßh to Em were rewritten so as to account for the observed effects of [Ko]. It is concluded that external potassium ions have an inactivating effect on the initial transient membrane conductance which cannot be explained solely on the basis of potassium membrane depolarization.

Role of Ba2+-resistant K+ channels in endothelium-dependent hyperpolarization of rat small mesenteric arteries

2004 ◽  
Vol 82 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Joke Breyne ◽  
Bert J Vanheel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electrical Response ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Combined Application ◽  
Junctional Coupling ◽  
A Minor

In rat small mesenteric arteries, the influence of modulation of basal smooth muscle K+ efflux on the mechanism of endothelium-dependent hyperpolarization was investigated. The membrane potentials of the vascular smooth muscle cells were measured using conventional microelectrode techniques. Incubation of resting arteries with the gap junction uncoupler carbenoxolone (20 µM) decreased the endothelium-dependent hyperpolarization elicited by a submaximal concentration of acetylcholine (3 µM) to about 65% of the control. In the presence of Ba2+ (200 µM), which depolarized the membrane potential by 10 mV, the acetylcholine-induced membrane potential response was doubled in magnitude, reaching values not different from control. Moreover, the hyperpolarization was more resistant to carbenoxolone in these conditions. Finally, both in the absence and in the presence of carbenoxolone, the combined application of Ba2+ and ouabain (0.5 mM) did not abolish the acetylcholine response. These results suggest that gap junctional coupling plays a role in endothelium-dependent hyperpolarization of smooth muscle cells of resting rat small mesenteric arteries. Additionally, these findings show that the hyperpolarization does not rely on activation of inward rectifying K+ channels. Although a minor contribution of Na–K pumping cannot be excluded, the Ba2+ experiments show that the membrane electrical response is mediated by activation of a Ba2+-resistant K+ conductance.Key words: EDHF, carbenoxolone, potassium channels, vascular smooth muscle cell membrane potential, vasodilation.

Sign in / Sign up

Export Citation Format

Share Document