Bioelectric Regulation of Tentacle Movement in a Dinoflagellate

1967 ◽  
Vol 47 (3) ◽  
pp. 433-446
Author(s):  
ROGER ECKERT ◽  
TAKAO SIBAOKA

1. Recurring extensions and flexions of the food-gathering tentacle of Noctiluca miliaris occur spontaneously. Identical movements can be evoked by appropriate electrical stimulation. 2. Spontaneous recurring potential wave forms (TRPs) were recorded from the vacuole of the luminescent form of Noctiluca during movements of the tentacle. The basic TRP wave form consists of a characteristic negative-going spike which arises at -20 to -30 mV. from the slowly redeveloping negativity of a pre-spike depolarization, and is followed by a quasi-stable post-spike d.c. level of relative vacuolar negativity (-45 to -60 mV.). 3. The TRP complex, similar in shape to that which occurs spontaneously, follows an intracellularly applied current pulse of either polarity if the vacuolar potential is at the post-spike level. The duration of the evoked pre-spike wave is related to the current intensity and duration. During the pre-spike state outward current is ineffective, although a TR spike occurs in response to inward current. 4. The TRP is distinct in its behaviour and wave form from the flash-triggering potential, which can be evoked in the same cell, even though both exhibit all-or-none spikes. 5. Simultaneous recordings of intracellular potentials and movements of the tentacle showed a consistent temporal relationship between potential changes and subsequent movement. Extension of the tentacle begins 1-2 sec. after the spike and flexion begins within 1 sec. after beginning of the pre-spike wave. 6. Tentacle movement ceased in Ca-free sea water even though the cyclic potential changes continued normally. 7. Electron micrographs of the tentacle showed longitudinal aggregations of microtubules near the outer surface of the peripheral cytoplasm. It is proposed that contraction of these microtubules is the immediate cause of tentacle movements.

1969 ◽  
Vol 59 (2) ◽  
pp. 865-908
Author(s):  
N. A. Haskell

abstract Displacement, particle velocity, and acceleration wave forms in the near field of a propagating fault have been computed by numerical integration of the Green's function integrals for an infinite medium. The displacement discontinuity (dislocation) on the fault plane is assumed to have the form of a unilaterally propagating finite ramp function in time. The calculated wave forms in the vicinity of the fault plane are quite similar to those observed at the strong motion station nearest the fault plane at the Parkfield earthquake. The comparison suggests that the propagating ramp time function is roughly representative of the main features of the dislocation motion on the fault plane, but that the actual motion has somewhat more high frequency complexity. Calculated amplitudes indicate that the average final dislocation on the fault at the Parkfield earthquake was more than an order of magnitude greater than the offsets observed on the visible surface trace. Computer generated wave form plots are presented for a variety of locations with respect to the fault plane and for two different assumptions on the relation between fault length and ramp function duration.


1999 ◽  
Vol 112 (23) ◽  
pp. 4425-4435 ◽  
Author(s):  
L.N. Naemsch ◽  
A.F. Weidema ◽  
S.M. Sims ◽  
T.M. Underhill ◽  
S.J. Dixon

Extracellular nucleotides act as signaling molecules in numerous tissues. In bone, nucleotides stimulate osteoclast formation and activity; however, the receptors and signaling mechanisms underlying these effects have yet to be identified. To identify specific P2X purinoceptor subtypes in osteoclasts, degenerate oligonucleotide primers were used to PCR-amplify DNA fragments from a rabbit osteoclast cDNA library. A 372-base-pair fragment was obtained that encoded an amino acid sequence with 88% identity to the rat P2X(4) purinoceptor. The presence of P2X(4) mRNA in purified osteoclasts was confirmed by reverse transcription-PCR. Endogenous purinoceptors were functionally characterized in isolated rabbit osteoclasts by patch-clamp recording in whole-cell configuration. At negative membrane potentials, application of ATP or ADP rapidly activated an inward current followed by an outward current. In contrast, UTP or ADPbetaS elicited only an outward current, due to activation of a Ca(2+)-dependent K(+) conductance. The initial inward current was non-selective for cations and inactivated during agonist application. Furthermore, the inward current was insensitive to suramin and Cibacron blue, and was potentiated by Zn(2+). These characteristics are consistent with properties of P2X(4) purinoceptors. Activation of P2X(4) purinoceptors leads to cation influx and depolarization. Nucleotides, released at sites of trauma or inflammation, may act through these receptors on osteoclasts to stimulate bone resorption.


1974 ◽  
Vol 64 (2) ◽  
pp. 473-491
Author(s):  
Harold M. Mooney

abstract We consider a version of Lamb's Problem in which a vertical time-dependent point force acts on the surface of a uniform half-space. The resulting surface disturbance is computed as vertical and horizontal components of displacement, particle velocity, acceleration, and strain. The goal is to provide numerical solutions appropriate to a comparison with observed wave forms produced by impacts onto granite and onto soil. Solutions for step- and delta-function sources are not physically realistic but represent limiting cases. They show a clear P arrival (larger on horizontal than vertical components) and an obscure S arrival. The Rayleigh pulse includes a singularity at the theoretical arrival time. All of the energy buildup appears on the vertical components and all of the energy decay, on the horizontal components. The effects of Poisson's ratio upon vertical displacements for a step-function source are shown. For fixed shear velocity, an increase of Poisson's ratio produces a P pulse which is larger, faster, and more gradually emergent, an S pulse with more clear-cut beginning, and a much narrower Rayleigh pulse. For a source-time function given by cos2(πt/T), −T/2 ≦ T/2, a × 10 reduction in pulse width at fixed pulse height yields an increase in P and Rayleigh-wave amplitudes by factors of 1, 10, and 100 for displacement, velocity and strain, and acceleration, respectively. The observed wave forms appear somewhat oscillatory, with widths proportional to the source pulse width. The Rayleigh pulse appears as emergent positive on vertical components and as sharp negative on horizontal components. We show a theoretical seismic profile for granite, with source pulse width of 10 µsec and detectors at 10, 20, 30, 40, and 50 cm. Pulse amplitude decays as r−1 for P wave and r−12 for Rayleigh wave. Pulse width broadens slightly with distance but the wave form character remains essentially unchanged.


1991 ◽  
Vol 260 (5) ◽  
pp. C934-C948 ◽  
Author(s):  
K. Kusano ◽  
H. Gainer

Voltage- and Ca(2+)-activated whole cell currents were studied in AR42J cells, a clonal cell line derived from rat pancreatic acinar cells, using a patch electrode voltage-clamp technique. Four kinds of ionic currents were identified by their ionic dependencies, pharmacological properties, and kinetic parameters: 1) an outward current flow due mainly to a voltage-dependent K(+)-conductance increase, 2) an initial transient inward current due to an Na(+)-conductance increase, 3) transient and long-duration inward current due to a Ca(2+)-conductance increase, and 4) a slowly activating inward current that persists over the duration of the depolarizing pulse and deactivates slowly upon repolarization, producing a slow inward tail current. The slow inward tail current was particularly robust and was interpreted as due to a Ca(2+)-activated Cl(-)-conductance increase, since 1) the generation of this current was blocked by removing the extracellular Ca2+, applying Ca(2+)-channel blockers (Cd2+, nifedipine), or by lowering the intracellular Ca2+ concentration [( Ca2+]i) with EGTA; and 2) the reversal potential (Erev) of the slow inward tail current was close to 0 mV in the control condition (152 mM [Cl-]o/154 mM [Cl-]i), and changes of the [Cl-]o/[Cl )i ratio shifted the Erev toward the predicted Cl- equilibrium potential.


1995 ◽  
Vol 74 (4) ◽  
pp. 1404-1420 ◽  
Author(s):  
R. M. Harris-Warrick ◽  
L. M. Coniglio ◽  
R. M. Levini ◽  
S. Gueron ◽  
J. Guckenheimer

1. The lateral pyloric (LP) neuron is a component of the 14-neuron pyloric central pattern generator in the stomatogastric ganglion of the spiny lobster, Panulirus interruptus. In the pyloric rhythm, this neuron fires rhythmic bursts of action potentials whose phasing depends on the pattern of synaptic inhibition from other network neurons and on the intrinsic postinhibitory rebound properties of the LP cell itself. Bath-applied dopamine excites the LP cell and causes its activity to be phase advanced in the pyloric motor pattern. At least part of this modulatory effect is due to dopaminergic modulation of the intrinsic rate of postinhibitory rebound in the LP cell. 2. The LP neuron was isolated from all detectable synaptic input. We measured the rate of recovery after 1-s hyperpolarizing current injections of varying amplitudes, quantifying the latency to the first spike following the hyperpolarizing prepulse and the interval between the first and second action potentials. Dopamine reduced both the first spike latency and the first interspike interval (ISI) in the isolated LP neuron. During the hyperpolarizating pre-steps, the LP cell showed a slow depolarizing sag voltage that was enhanced by dopamine. 3. We used voltage clamp to analyze dopamine modulation of subthreshold ionic currents whose activity is affected by hyperpolarizing prepulses. Dopamine modulated the transient potassium current IA by reducing its maximal conductance and shifting its voltage dependence for activation and inactivation to more depolarized voltages. This outward current is normally transiently activated after hyperpolarization of the LP cell, and delays the rate of postinhibitory rebound; by reducing IA, dopamine thus accelerates the rate of rebound of the LP neuron. 4. Dopamine also modulated the hyperpolarization-activated inward current Ih by shifting its voltage dependence for activation 20 mV in the depolarizing direction and accelerating its rate of activation. This enhanced inward current helps accelerate the rate of rebound in the LP cell after inhibition. 5. The relative roles of Ih and IA in determining the first spike latency and first ISI were explored using pharmacological blockers of Ih (Cs+) and IA [4-aminopyridine (4-AP)]. Blockade of Ih prolonged the first spike latency and first ISI, but only slightly reduced the net effect of dopamine. In the continued presence of Cs+, blockade of IA with 4-AP greatly shortened the first spike latency and first ISI. Under conditions where both Ih and IA were blocked, dopamine had no additional effect on the LP cell. 6. We used the dynamic clamp technique to further study the relative roles of IA and Ih modulation in dopamine's phase advance of the LP cell. We blocked the endogenous Ih with Cs+ and replaced it with a simulated current generated by a computer model of Ih. The neuron with simulated Ih gave curves relating the hyperpolarizing prepulse amplitude to first spike latency that were the same as in the untreated cell. Changing the computer parameters of the simulated Ih to those induced by dopamine without changing IA caused only a slight reduction in first spike latency, which was approximately 20% of the total reduction caused by dopamine in an untreated cell. Bath application of dopamine in the presence of Cs+ and simulated Ih (with control parameters) allowed us to determine the effect of altering IA but not Ih: this caused a significant reduction in first spike latency, but it was still only approximately 70% of the effect of dopamine in the untreated cell. Finally, in the continued presence of dopamine, changing the parameters of the simulated Ih to those observed with dopamine reduced the first spike latency to that seen with dopamine in the untreated cell. 7. We generated a mathematical model of the lobster LP neuron, based on the model of Buchholtz et al. for the crab LP neuron.


2014 ◽  
Vol 143 (4) ◽  
pp. 449-464 ◽  
Author(s):  
Natascia Vedovato ◽  
David C. Gadsby

A single Na+/K+-ATPase pumps three Na+ outwards and two K+ inwards by alternately exposing ion-binding sites to opposite sides of the membrane in a conformational sequence coupled to pump autophosphorylation from ATP and auto-dephosphorylation. The larger flow of Na+ than K+ generates outward current across the cell membrane. Less well understood is the ability of Na+/K+ pumps to generate an inward current of protons. Originally noted in pumps deprived of external K+ and Na+ ions, as inward current at negative membrane potentials that becomes amplified when external pH is lowered, this proton current is generally viewed as an artifact of those unnatural conditions. We demonstrate here that this inward current also flows at physiological K+ and Na+ concentrations. We show that protons exploit ready reversibility of conformational changes associated with extracellular Na+ release from phosphorylated Na+/K+ pumps. Reversal of a subset of these transitions allows an extracellular proton to bind an acidic side chain and to be subsequently released to the cytoplasm. This back-step of phosphorylated Na+/K+ pumps that enables proton import is not required for completion of the 3 Na+/2 K+ transport cycle. However, the back-step occurs readily during Na+/K+ transport when external K+ ion binding and occlusion are delayed, and it occurs more frequently when lowered extracellular pH raises the probability of protonation of the externally accessible carboxylate side chain. The proton route passes through the Na+-selective binding site III and is distinct from the principal pathway traversed by the majority of transported Na+ and K+ ions that passes through binding site II. The inferred occurrence of Na+/K+ exchange and H+ import during the same conformational cycle of a single molecule identifies the Na+/K+ pump as a hybrid transporter. Whether Na+/K+ pump–mediated proton inflow may have any physiological or pathophysiological significance remains to be clarified.


1999 ◽  
Vol 81 (2) ◽  
pp. 535-543 ◽  
Author(s):  
Erik P. Cook ◽  
Daniel Johnston

Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input. We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both αamino-3-hydroxy-5-methyl-4-isoxazolepropionic acid– and N-methyl-d-aspartate–like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials.


1990 ◽  
Vol 151 (1) ◽  
pp. 21-39 ◽  
Author(s):  
JONATHAN A. DAVID ◽  
DAVID B. SATTELLE

The ionic basis of the resting potential and of the response to acetylcholine (ACh) has been investigated in the cell body membrane of the fast coxal depressor motor neurone in the metathoracic ganglion of the cockroach Periplaneta americana. By means of ion-sensitive microelectrodes, intracellular concentrations of three ion species were estimated (mmoll−1): [K+]i, 1443; [Na+]i, 9±1; [Cl−], 7±1. The resting potential of continuously superfused cells was −75.6±1.9mV at 22° C. A change in resting potential of 42.0±2.5mV accompanied a decade change in [K+]o. Experiments with (10−4moll−1) ouabain, Na+ injection, low temperature (10°C) and non-superfused cells indicated the presence of an electrogenic sodium pump. Under current-clamp, the cell body membrane was depolarized by sequentially applied, ionophoretic pulses (500ms duration) of ACh. Under voltage-clamp, such doses of ACh resulted in an inward current which was abolished in low-Na+ saline. Ion-sensitive electrodes revealed an increase in [Na+]i but no change in [Cl−1]j in response to externally applied ACh. The ACh-induced current-voltage relationship was shifted in a negative direction by low-K+ saline. The AChinduced inward current was usually followed by a delayed outward current which reversed at Ek. Low-K+ saline had the same effect on this outward component as depolarizing the membrane. This suggests that the outward current component is carried by K+. The ACh-induced inward current and the delayed outward current were potentiated either when [Ca2+]i was lowered by injecting the calcium chelator BAPTA or by exposure of the cell to low-Ca2+ saline. High-Ca2+ saline reduced the inward component of the response and produced a negative shift in the AChinduced current-voltage relationship. The amplitude of the delayed outward


1988 ◽  
Vol 66 (2) ◽  
pp. 222-232 ◽  
Author(s):  
Magda Horackova ◽  
Andrzej Beresewicz ◽  
Gerrit Isenberg

We have studied changes in electrical activity resulting from abrupt alterations of the Na gradient, using ventricular myocytes isolated from feline and bovine hearts. Attempting to investigate the ionic current possibly generated by Na–Ca exchange, we studied the effects of the changes in [Na]o in the presence of 20 mM CsCl to inhibit K currents. To facilitate the effect of Cs, we also used a K-free solution and a patch electrode filled with 150 mM cesium glutamate. The application of 20 mM Nao resulted in hyperpolarization and the action potential duration was reduced. Under voltage clamp, 20 or 45 mM Nao generated an outward current at all membrane potentials investigated. The initial part (100–200 ms) of this current was only partially inhibited by 5 mM NiCl2 which is known to fully block the Ca inward current. However, the outward current generated by the reduced [Na]o was fully inhibited by 20 mM MnCl2 (which presumably inhibits Na–Ca exchange). Our observations extend the work on multicellular cardiac preparations indicating that the outward current elicited by a sudden decrease in Na gradient could be generated by Na–Ca exchange. Although the characteristics of this outward current support certain concepts of the Na–Ca exchange in cardiac muscle, we cannot at present exclude a contribution of other membrane current(s).


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