Steady-state point-source stimulation of a nerve containing axons with an arbitrary distribution of diameters

1992 ◽  
Vol 30 (1) ◽  
pp. 103-108 ◽  
Author(s):  
B. J. Roth ◽  
K. W. Altman
Keyword(s):  
Steady State ◽  
Point Source ◽  
Arbitrary Distribution ◽  
State Point ◽  
Stimulation Of

Surface displacements due to an underground explosion

1966 ◽  
Vol 56 (4) ◽  
pp. 877-888
Author(s):  
G. N. Bycroft
Keyword(s):  
Steady State ◽  
Point Source ◽  
Spherical Cavity ◽  
Nuclear Explosion ◽  
Elastic Half Space ◽  
Underground Explosion ◽  
Maximum Displacement ◽  
Surface Displacements ◽  
State Point ◽  
Transient Case

abstract A simple solution to the problem of the surface displacements on an elastic half-space caused by an underground explosion is presented. The analysis is based on deriving the transient case for a point source from the steady state point source and then proceeding to the case of a finite spherical cavity by means of a retarded potential. Theoretical values of maximum displacement compare favorably with measured values from the underground test shot Rainier, a nuclear explosion of Operation Plumbob.

Steady-State Point-Source Excitation of a Laminated Composite

1983 ◽  
Vol 50 (1) ◽  
pp. 165-168
Author(s):  
G. S. Beaupre ◽  
G. Herrmann
Keyword(s):  
Steady State ◽  
Point Source ◽  
Group Velocity ◽  
Laminated Composite ◽  
Periodic Excitation ◽  
Geometric Optics ◽  
Antiplane Strain ◽  
State Point ◽  
Elastic Composite ◽  
Source Excitation

Steady-state periodic excitation at a point of an extended, periodically laminated, elastic composite is considered in antiplane strain. The curves of constant phase are determined in the geometric optics approximation. The associated distribution of group velocity is also calculated.

scholarly journals Receptor-operated Ca2+ channels in gastric parietal cells: gastrin and carbachol induce Ca2+ influx in depleting intracellular Ca2+ stores

1993 ◽  
Vol 289 (1) ◽  
pp. 117-124 ◽  
Author(s):  
S Roche ◽  
J P Bali ◽  
R Magous
Keyword(s):  
Steady State ◽  
Receptor Activation ◽  
Parietal Cells ◽  
The Other ◽  
Bivalent Cation ◽  
Gtp Binding ◽  
Gastric Parietal Cells ◽  
Type Receptor ◽  
Ca2 Channels ◽  
Stimulation Of

The mechanism whereby gastrin-type receptor and muscarinic M3-type receptor regulate free intracellular Ca2+ concentration ([Ca2+]i) was studied in rabbit gastric parietal cells stimulated by either gastrin or carbachol. Both agonists induced a biphasic [Ca2+]i response: a transient [Ca2+]i rise, followed by a sustained steady state depending on extracellular Ca2+. Gastrin and carbachol also caused a rapid and transient increase in Mn2+ influx (a tracer for bivalent-cation entry). Pre-stimulation of cells with one agonist drastically decreased both [Ca2+]i increase and Mn2+ influx induced by the other. Neither diltiazem nor pertussistoxin treatment had any effect on agonist-stimulated Mn2+ entry. Thapsigargin, a Ca(2+)-pump inhibitor, induced a biphasic [Ca2+]i increase, and enhanced the rate of Mn2+ entry. Preincubation of cells with thapsigargin inhibits the [Ca2+]i increase as well as Mn2+ entry stimulated by gastrin or by carbachol. Thapsigargin induced a weak but significant increase in Ins(1,4,5)P3 content, but this agent had no effect on the agonist-evoked Ins(1,4,5)P3 response. In permeabilized parietal cells, Ins(1,4,5)P3 and caffeine caused an immediate Ca2+ release from intracellular pools, followed by a reloading of Ca2+ pools which can be prevented in the presence of thapsigargin. We conclude that (i) gastrin and carbachol mobilize common Ca2+ intracellular stores, (ii) Ca2+ permeability secondary to receptor activation involves neither a voltage-sensitive Ca2+ channel nor a GTP-binding protein from the G1 family, and (iii) agonists regulate common Ca2+ channels in depleting intracellular Ca2+ stores.

Steady-state point-defect diffusion profiles in solids during irradiation

1974 ◽  
Vol 23 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Nghi Q. Lam ◽  
Steven J. Rothman ◽  
Rudolf Sizmanns
Keyword(s):  
Steady State ◽  
Point Defect ◽  
Defect Diffusion ◽  
State Point ◽  
Diffusion Profiles

Tetanic hyperpolarization of single medullated nerve fibers in sodium and lithium

1976 ◽  
Vol 231 (4) ◽  
pp. 1033-1038 ◽  
Author(s):  
GM Schoepfle
Keyword(s):  
Steady State ◽  
Interspike Interval ◽  
Nerve Fibers ◽  
Repetitive Stimulation ◽  
Time Dependent ◽  
Potassium Ions ◽  
Current Densities ◽  
Medullated Nerve Fiber ◽  
Sodium And Potassium ◽  
Stimulation Of

Repetitive stimulation of a single medullated nerve fiber of Xenopus yields a succession of postspike voltage-time curves which are nearly coincident until attainment of a voltage that corresponds to that of the maximum attained by the normal postspike undershoot. Initially the interspike potential returns toward a resting level after this brief phase of hyperpolarization. However, as tetanization proceeds, a pattern of hyperpolarization develops with the result that, in the tetanic steady state, there exists a progressive hyperpolarization throughout each interspike interval. Extent of postspike hyperpolarization in terms of a deviation deltaVm from the resting level of membrane potential is approximated by the variation deltaVm = delta[MNa + MK]/[GNa + GK] where MNa and MK are current densities associated with active pumping of sodium and potassium ions and GNa and GK are corresponding time-dependent leak conductances. Tetanic hyperpolarization is reversibly abolished by cyanide and by exposure to lithium Ringer. Eventual reappearance of tetanic hyperpolarization in the presence of lithium Ringer suggests lithium pumping.

scholarly journals The "late" Ca channel in squid axons.

1981 ◽  
Vol 78 (6) ◽  
pp. 683-700 ◽  
Author(s):  
L J Mullins ◽  
J Requena
Keyword(s):  
Steady State ◽  
Repetitive Stimulation ◽  
Test Solution ◽  
Ca Channel ◽  
Normal Concentration ◽  
Giant Axons ◽  
Light Production ◽  
High K ◽  
K Response ◽  
Stimulation Of

Squid giant axons were injected with aequorin and then treated with seawater containing 50 mM Ca and 100-465 mM K+. Measurements of light production suggested a phasic entry of Ca as well as an enhanced steady-state aequorin glow. After a test K+ depolarization, the aequorin-injected axon was stimulated for 30 min in Li seawater that was Ca-free, a procedure known to reduce [Na]i to about one-half the normal concentration. Reapplication of the elevated K+ test solution now showed that the Ca entry was virtually abolished by this stimulation in Li. A subsequent stimulation of the axon in Na seawater for 30 min resulted in recovery of the response to depolarization by high K+ noted in a normal fresh axon. In axons first tested for a high K+ response and then stimulated in Na seawater for 30 min (where [Na]i increases approximately 30%), there was approximately eight fold enhancement in this response to a test polarization. Axons depolarized with 465 mM K seawater in the absence of external Ca for several minutes were still capable of producing a large phasic entry of Ca when [Ca]0 was made 50 mM, which suggests that it is Ca entry itself rather than membrane depolarization that produced inactivation. Responses to stimulation at 60 pulses/s in Na seawater containing 50 mM Ca are at best only 5% of those measured with high K solutions. The response to repetitive stimulation is not measurable if [Ca]o is made 1 mM, whereas the response to steady depolarization is scarcely affected.

scholarly journals High-density EEG of auditory steady-state responses during stimulation of basal forebrain parvalbumin neurons

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Eunjin Hwang ◽  
Hio-Been Han ◽  
Jung Young Kim ◽  
Jee Hyun Choi
Keyword(s):  
Steady State ◽  
Basal Forebrain ◽  
Event Related Potentials ◽  
High Density ◽  
Time Stamps ◽  
Related Potentials ◽  
Steady State Responses ◽  
Auditory Steady State Responses ◽  
State Responses ◽  
Stimulation Of

Abstract We present high-density EEG datasets of auditory steady-state responses (ASSRs) recorded from the cortex of freely moving mice with or without optogenetic stimulation of basal forebrain parvalbumin (BF-PV) neurons, known as a subcortical hub circuit for the global workspace. The dataset of ASSRs without BF-PV stimulation (dataset 1) contains raw 36-channel EEG epochs of ASSRs elicited by 10, 20, 30, 40, and 50 Hz click trains and time stamps of stimulations. The dataset of ASSRs with BF-PV stimulation (dataset 2) contains raw 36-channel EEG epochs of 40-Hz ASSRs during BF-PV stimulation with latencies of 0, 6.25, 12.5, and 18.75 ms and time stamps of stimulations. We provide the datasets and step-by-step tutorial analysis scripts written in Python, allowing for descriptions of the event-related potentials, spectrograms, and the topography of power. We complement this experimental dataset with simulation results using a time-dependent perturbation on coupled oscillators. This publicly available dataset will be beneficial to the experimental and computational neuroscientists.

pH regulation and response to AVP in A10 cells differ markedly in the presence vs. absence of CO2-HCO3-

1990 ◽  
Vol 259 (3) ◽  
pp. C471-C483 ◽  
Author(s):  
D. Kikeri ◽  
M. L. Zeidel ◽  
B. J. Ballermann ◽  
B. M. Brenner ◽  
S. C. Hebert
Keyword(s):  
Steady State ◽  
Ph Regulation ◽  
Disulfonic Acid ◽  
Potential Contribution ◽  
Vasoactive Agents ◽  
Cell Responses ◽  
Extrusion Mechanism ◽  
Acid Extrusion ◽  
Ambient Co2 ◽  
Stimulation Of

The fluorescent pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF) was used to determine the effect of ambient CO2-HCO3- on the regulation of intracellular pH (pHi) and the pHi response to arginine vasopressin (AVP) in A10 vascular smooth muscle (VSM) cells. Steady-state pHi averaged 7.04 +/- 0.02 in the absence and 7.25 +/- 0.01 in the presence of CO2-HCO3-. In the absence of CO2-HCO3-, virtually all (greater than 96%) of the acid extrusion from acidification occurred by amiloride-sensitive Na(+)-H+ exchange. However, in the presence of CO2-HCO3-, acid extrusion after acidification occurred by both Na(+)-H+ exchange and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-sensitive Na(+)-dependent Cl(-)-HCO3- exchange. In CO2-HCO3(-)-containing media, amiloride-sensitive Na(+)-H+ exchange mediated 85% of acid extrusion at a pHi of 6.48, but the DIDS-sensitive acid extrusion mechanism (NA(+)-dependent Cl(-)-HCO3- exchange) was the dominant acid extrusion mechanism at a pHi of 6.94. Base exited A10 cells by a DIDS-sensitive process consistent with Na(+)-independent Cl(-)-HCO3- exchange. Both amiloride- and DIDS-sensitive processes regulated steady-state pHi in CO2-HCO3-. AVP (10(-7) M) alkalinized steady-state pHi in the absence of CO2-HCO3- (delta pHi = 0.08 +/- 0.01 pH units) by stimulating Na(+)-H+ exchange; however, AVP did not alter pHi of untreated cells in CO2-HCO3- (delta pHi = -0.01 +/- 0.01 pH units) because of concomitant stimulation of Na(+)-independent Cl(-)-HCO3-exchange. We conclude that the steady-state pHi, the mechanisms of pHi regulation, and the pHi response to AVP in A10 cells are critically influenced by the presence of extracellular CO2-HCO3-. Thus the potential contribution of pHi changes to VSM cell responses to vasoactive agents should be evaluated in the presence of CO2-HCO3-.

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