Tetanic hyperpolarization of single medullated nerve fibers in sodium and lithium

1976 ◽  
Vol 231 (4) ◽  
pp. 1033-1038 ◽  
Author(s):  
GM Schoepfle

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.

1981 ◽  
Vol 78 (6) ◽  
pp. 683-700 ◽  
Author(s):  
L J Mullins ◽  
J Requena

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.


2020 ◽  
Author(s):  
Zhou Yu ◽  
J. Michael McIntosh ◽  
Soroush Sadeghi ◽  
Elisabeth Glowatzki

ABSTRACTIn the vestibular peripheral organs, type I and type II hair cells (HCs) transmit incoming signals via glutamatergic quantal transmission onto afferent nerve fibers. Additionally, type I HCs transmit via ‘non-quantal’ transmission to calyx afferent fibers, by accumulation of glutamate and potassium in the synaptic cleft. Vestibular efferent inputs originating in the brainstem contact type II HCs and vestibular afferents. Here, we aimed at characterizing the synaptic efferent inputs to type II HCs using electrical and optogenetic stimulation of efferent fibers combined with in vitro whole-cell patch clamp recording from type II HCs in the rodent vestibular crista. Properties of efferent synaptic currents in type II HCs were similar to those found in cochlear hair cells and mediated by activation of α9/α10 nicotinic acetylcholine receptors (AChRs) and SK potassium channels. While efferents showed a low probability of release at low frequencies of stimulation, repetitive stimulation resulted in facilitation and increased probability of release. Notably, the membrane potential of type II HCs measured during optogenetic stimulation of efferents showed a strong hyperpolarization even in response to single pulses and was further enhanced by repetitive stimulation. Such efferent-mediated inhibition of type II HCs can provide a mechanism to adjust the contribution of signals from type I and type II HCs to vestibular nerve fibers. As a result, the relative input of type I hair cells to vestibular afferents will be strengthened, emphasizing the phasic properties of the incoming signal that are transmitted via fast non-quantal transmission.New and NoteworthyType II vestibular hair cells (HCs) receive inputs from efferent fibers originating in the brainstem. We used in vitro optogenetic and electrical stimulation of efferent fibers to study their synaptic inputs to type II HCs. Efferent inputs inhibited type II HCs, similar to cochlear efferent effects. We propose that efferent inputs adjust the contribution of signals from type I and type II HCs that report different components of the incoming signal to vestibular nerve fibers.


1976 ◽  
Vol 231 (2) ◽  
pp. 449-453 ◽  
Author(s):  
U Proske ◽  
PM Rack

The semitendinous muscle of the lizard Tilique contains both slow and twitch fibers; by subdivision of its motor nerve, fibers of each type may be stimulated separately. When, during repetitive stimulation of nerve filaments, the muscle was lengthened or shortened, the tension changes included an initial short-range stiffness, followed by a later compliance. With increasing velocities of movement, the short-range stiffness increased toward a limiting value. For slow fibers this limiting value was reached with lower velocities of movement than for the twitch fibers. Provided that the same velocity of movement was used and the movements began from similar initial isometric tensions, the slow fibers resisted the movements with a greater stiffness than the twitch fibers. It is suggested that not all of the observed differences between the two fiber types can be interpreted simply in terms of differences in rates of formation and breakdown of cross-links.


1937 ◽  
Vol 73 (2) ◽  
pp. 237-241 ◽  
Author(s):  
C. LADD PROSSER ◽  
JOHN Z. YOUNG

1984 ◽  
Vol 40 ◽  
Author(s):  
R. E. Benenson ◽  
P. Berning ◽  
L. Wielunski

AbstractLateral concentration profiles of hydrogen (1H) have been measured using nuclear recoil analysis on electrolytically charged metal (V, Nb, Ta) foils subjected to current densities of order 103 amps/cm2 for various times in order to study the electromigration of hydrogen. Initially uniformly loaded foils exhibited a dramatic redistribution of the hydrogen. Numerical analysis of these data using the conventional solution of the electromigration equation is used to extract the hydrogen effective charge (Z*) from the steady state data and the diffusion coefficient from the time-dependent data. The nuclear technique permits rapid and accurate direct concentration measurements capable of distinguishing surface and subsurface transport.


1990 ◽  
Vol 258 (4) ◽  
pp. C618-C621
Author(s):  
E. Bozler

Isometric and isotonic contractions of the tonus fibers of the frog were recorded using anodal block of the nerve fibers of the twitch fibers. Repetitive stimulation produced a contraction with a very slow rising phase because the individual responses were very weak. The first two or three stimuli usually did not give a visible response at all. However, if the twitch fibers were also stimulated, the responses of the tonus fibers were many times stronger and faster, but only under isotonic conditions. This indicates that the large increase in the responses of the tonus fibers was produced by the passive shortening caused by the contraction of the twitch fibers. A strong and fast response of the tonus fibers was also obtained if during stimulation of the tonus fibers the muscle was made to shorten by diminishing the load. It is suggested that the enormous effect of shortening is due to the regenerating action of shortening previously demonstrated.


1993 ◽  
Vol 289 (1) ◽  
pp. 117-124 ◽  
Author(s):  
S Roche ◽  
J P Bali ◽  
R Magous

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.


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