scholarly journals Electrophysiological Control of Reversed Ciliary Beating in Paramecium

1973 ◽  
Vol 61 (5) ◽  
pp. 572-587 ◽  
Author(s):  
Hans Machemer ◽  
Roger Eckert
Keyword(s):  
Membrane Potential ◽  
Electric Stimulation ◽  
Surface Membrane ◽  
Progressive Increase ◽  
Membrane Depolarization ◽  
Equilibrium Potential ◽  
Positive Potential ◽  
Ciliary Beating ◽  
Current Pulses ◽  
Ciliary Reversal

Quantitative relations between ciliary reversal and membrane responses were examined in electrically stimulated paramecia. Specimens bathed in 1 mM CaCl2, 1 mM KCl, and 1 mM Tris-HCl, pH 7.2, were filmed at 250 frames per second while depolarizing current pulses were injected. At current intensities producing only electrotonic shifts the cilia failed to respond. Stimuli which elicited a regenerative response were followed by a period of reversed ciliary beating. With increasing stimulus intensities the latency of ciliary reversal dropped from 30 to 4 ms or less, and the duration of reversal increased from 50 ms to 2.4 s or more; the corresponding regenerative responses increased in amplitude and rate of rise. With progressively larger intracellular positive pulses, electric stimulation became less effective, producing responses with a progressive increase in latency and decrease in duration of reversed beating of the cilia. When 100-ms pulses shifted the membrane potential to +70 mV or more, ciliary reversal was suppressed until the end of the pulse. "Off" responses then occurred with a latency of 2–4 ms independent of further increases in positive potential displacement. These results suggest that ciliary reversal is coupled to membrane depolarization by the influx of ions which produces the regenerative depolarization of the surface membrane. According to this view suppression of the ciliary response during stimulation occurs when the membrane potential approaches the equilibrium potential of the coupling ion, thereby retarding its influx. Previous data together with the present findings suggest that this ion is Ca2+.

Role of the Cilia Membrane in Control of Microtubule Sliding

1980 ◽  
Vol 38 ◽  
pp. 612-615
Author(s):  
Edna S. Kaneshiro
Keyword(s):  
Control Mechanism ◽  
Beat Frequency ◽  
Surface Membrane ◽  
Ciliary Membrane ◽  
Ciliary Beating ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
Reversal Mechanism ◽  
And Function

It is currently believed that ciliary beating results from microtubule sliding which is restricted in regions to cause bending. Cilia beat can be modified to bring about changes in beat frequency, cessation of beat and reversal in beat direction. In ciliated protozoans these modifications which determine swimming behavior have been shown to be related to intracellular (intraciliary) Ca2+ concentrations. The Ca2+ levels are in turn governed by the surface ciliary membrane which exhibits increased Ca2+ conductance (permeability) in response to depolarization. Mutants with altered behaviors have been isolated. Pawn mutants fail to exhibit reversal of the effective stroke of ciliary beat and therefore cannot swim backward. They lack the increased inward Ca2+ current in response to depolarizing stimuli. Both normal and pawn Paramecium made leaky to Ca2+ by Triton extrac¬tion of the surface membrane exhibit backward swimming only in reactivating solutions containing greater than IO-6 M Ca2+ Thus in pawns the ciliary reversal mechanism itself is left operational and only the control mechanism at the membrane is affected. The topographic location of voltage-dependent Ca2+ channels has been identified as a component of the ciliary mem¬brane since the inward Ca2+ conductance response is eliminated by deciliation and the return of the response occurs during cilia regeneration. Since the ciliary membrane has been impli¬cated in the control of Ca2+ levels in the cilium and therefore is the site of at least one kind of control of microtubule sliding, we have focused our attention on understanding the structure and function of the membrane.

Membrane Control of Ciliary Activity in the Protozoan Euplotes

1973 ◽  
Vol 58 (2) ◽  
pp. 437-462
Author(s):  
MILES EPSTEIN ◽  
ROGER ECKERT
Keyword(s):  
Membrane Potential ◽  
Normal Direction ◽  
Direct Access ◽  
Ciliary Activity ◽  
Cell Interior ◽  
Ciliary Beating ◽  
Ciliary Reversal ◽  
Intracellular Ca ◽  
Triton X ◽  
External Calcium

1. Membrane control of ciliary activity in the protozoan Euplotes was investigated by a combination of electrophysiological and cinematographic techniques. 2. The anal cirri, which are quiescent in the absence of stimulation, were selected for this study. 3. Membrane depolarization by means of injected current produced a reversal of the direction of beating (i.e. towards the cell anterior so as to make the ciliate swim backwards). Depolarization also increased the frequency of beating. Increasing depolarizations resulted in an increased number of reversed beats and increased frequency. 4. When the membrane potential was shifted beyond +70 mV, reversed beating did not occur until after the current pulse ended. 5. Depolarization did not evoke reversed beating when the external calcium (Ca) concentration was reduced to 10-6 M with EGTA. 6. Hyperpolarization caused the cirri to beat in a normal direction (i.e. towards the rear of the ciliate so as to cause the animal to swim forward). Increasing hyperpolarizations resulted in an increased number of forward beats and an increased frequency. 7. The cell was treated with the detergent Triton X-100 to permit Ca, Mg and ATP direct access through the extracted membrane to the cell interior. At Ca concentrations below 10-7 M, Mg-ATP-reactivated cilia of Triton-extracted cells beat normally. At Ca concentrations above approximately 10-7 M the reactivated beat resembled the reversed beat in the living cell. 8. The evidence suggests that membrane-regulated concentrations of intracellular Ca control the direction of ciliary beating. Thus, stimuli which produce an adequate Ca influx lead to ciliary reversal.

Characterization of synaptically mediated fast and slow inhibitory processes in piriform cortex in an in vitro slice preparation

1988 ◽  
Vol 59 (5) ◽  
pp. 1352-1376 ◽  
Author(s):  
G. F. Tseng ◽  
L. B. Haberly
Keyword(s):  
Membrane Potential ◽  
Piriform Cortex ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Membrane Depolarization ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Pentobarbital Sodium ◽  
Postsynaptic Potential ◽  
Conductance Increase

1. Intracellular recordings were obtained from anatomically verified layer II pyramidal cells in slices from rat piriform cortex cut perpendicular to the surface. 2. Responses to afferent and association fiber stimulation at resting membrane potential consisted of a depolarizing potential followed by a late hyperpolarizing potential (LHP). Membrane polarization by current injection revealed two components in the depolarizing potential: an initial excitatory postsynaptic potential (EPSP) followed at brief latency by an inhibitory postsynaptic potential (IPSP) that inverted with membrane depolarization and truncated the duration of the EPSP. 3. The early IPSP displayed the following characteristics suggesting mediation by gamma-aminobutyric acid (GABA) receptors linked to Cl- channels: associated conductance increase, sensitivity to increases in internal Cl- concentration, blockage by picrotoxin and bicuculline, and potentiation by pentobarbital sodium. The reversal potential was in the depolarizing direction with respect to resting membrane potential so that the inhibitory effect was exclusively via current shunting. 4. The LHP had an associated conductance increase and a reversal potential of -90 mV in normal bathing medium that shifted according to Nernst predictions for a K+ potential with changes in external K+ over the range 4.5-8 mM indicating mediation by the opening of K+ channels and ruling out an electrogenic pump origin. 5. Lack of effect of bath-applied 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) or internally applied ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) on the LHP and failure of high amplitude, direct membrane depolarization to evoke a comparable potential, argue against endogenous mediation of the LHP by a Ca2+ activated K+ conductance [gK(Ca)]. However, an apparent endogenously mediated gK(Ca) with a duration much greater than the LHP was observed in a low percent of layer II pyramidal cells. Lack of effect of 8-Br-cAMP also indicates a lack of dependence of the LHP on cAMP. 6. Other characteristics of the LHP that were demonstrated include: a lack of blockage by GABAA receptor antagonists, a probable voltage sensitivity (decrease in amplitude in the depolarizing direction), and an apparent brief onset latency (less than 10 ms) when the early IPSP was blocked by picrotoxin. The LHP was unaffected by pentobarbital sodium when the early IPSP was blocked by picrotoxin. 7. Both the LHP and early IPSP were blocked by low Ca2+/high Mg2+, consistent with disynaptic mediation.(ABSTRACT TRUNCATED AT 400 WORDS)

Beta-adrenergic actions on membrane electrical properties of dissociated smooth muscle cells

1988 ◽  
Vol 254 (3) ◽  
pp. C423-C431 ◽  
Author(s):  
H. Yamaguchi ◽  
T. W. Honeyman ◽  
F. S. Fay
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Beta Adrenergic

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of intracellular potassium and sodium injections on the inhibitory postsynaptic potential

1964 ◽  
Vol 160 (979) ◽  
pp. 181-196 ◽  
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Direct Evidence ◽  
Equilibrium Potential ◽  
Ionic Mechanism ◽  
Half Time ◽  
Intracellular Potassium ◽  
Postsynaptic Potential ◽  
Almost All

Two barrels of double microelectrodes have been filled with different salts so that the electrophoretic injection of Na + and K + ions could be investigated in alternating sequence on the same motoneuron in the cat spinal cord. The effects of these injections on the mechanism generating the IPSP were evaluated by determining the equilibrium potential for the IPSP (the E IPSP ), i. e. the membrane potential at which the IPSP is zero. Such determinations have been made every 5 to 10 s after ion injections and have provided the most direct evidence of the ionic mechanism generating the IPSP . Comparison of the Na + and K + ion injections shows that the former injection always displaced the E IPSP much farther in the depolarizing direction and that recovery was much slower, with a half-time of 70 to 120 s, in contrast to about 20 s after the K + injection. In the discussion and evaluation of these results it was postulated that almost all of the displacement of the E IPSP in the depolarizing direction was due to the increased intracellular Cl - concentration, the (Cl - ) i . Under normal conditions a high (Cl - ) i declines by diffusional exchange across the cell membrane with a half-time of about 20 s, but this decline is much slower when the internal potassium is depleted. An explanation of this difference will be given in the following paper.

scholarly journals Nukacin ISK-1, a Bacteriostatic Lantibiotic

2009 ◽  
Vol 53 (8) ◽  
pp. 3595-3598 ◽  
Author(s):  
Sikder M. Asaduzzaman ◽  
Jun-ichi Nagao ◽  
Hiroshi Iida ◽  
Takeshi Zendo ◽  
Jiro Nakayama ◽  
...  
Keyword(s):  
Cell Wall ◽  
Membrane Potential ◽  
Bacterial Strain ◽  
Mode Of Action ◽  
Membrane Depolarization ◽  
Wall Width ◽  
Cytoplasmic Content ◽  
Remarkable Reduction

ABSTRACT We determined the mode of action of nukacin ISK-1. It did not cause membrane potential dissipation or the efflux of ATP or K+ ions from the cells of a sensitive bacterial strain; however, it blocked the membrane depolarization activity of nisin. Nukacin ISK-1-treated cells had single arrangements of cells without the formation of a complete septum. A remarkable reduction in cell wall width was also observed, but cytoplasmic content was unaffected. We concluded that nukacin ISK-1 is bacteriostatic.

scholarly journals Role of sodium in ADP- and thrombin-induced megakaryocyte spreading.

1983 ◽  
Vol 96 (5) ◽  
pp. 1234-1240 ◽  
Author(s):  
R M Leven ◽  
W H Mullikin ◽  
V T Nachmias
Keyword(s):  
Membrane Potential ◽  
Intracellular Recording ◽  
Membrane Depolarization ◽  
Sodium Permeability ◽  
Sodium Conductance ◽  
Extracellular Sodium

We investigated the role of sodium in megakaryocyte spreading induced by thrombin and ADP. We found that if extracellular sodium was replaced by lithium, potassium, or choline, spreading was inhibited. When extracellular sodium was present, amiloride or tetrodotoxin inhibited spreading. Using intracellular recording we found spreading to be associated with a permanent membrane depolarization. The extent and rate of thrombin-induced depolarization was reduced when lithium replaced sodium. Unspread cells had an average membrane potential of -44.8 mV. Spread cells had an average membrane potential of -18.46 mV. When choline replaced sodium, or when in the presence of tetrodotoxin and amiloride, the spread cells repolarized, indicating that the depolarization is due to an increase in sodium permeability. Similar treatments did not change the membrane potential of unspread cells. Incubation of megakaryocytes with A23187 together with monensin or methylamine induced spreading. Methylamine occasionally caused spreading by itself, but neither ionophore alone caused spreading. These results indicate that megakaryocyte spreading induced by ADP and thrombin depends on an increase in sodium conductance.

Cellular and subcellular mechanisms of cardiac pacemaker oscillations

1979 ◽  
Vol 81 (1) ◽  
pp. 205-215
Author(s):  
R. W. Tsien ◽  
R. S. Kass ◽  
R. Weingart
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Surface Membrane ◽  
Cardiac Pacemaker ◽  
Oscillatory Activity ◽  
Purkinje Fibre ◽  
Pacemaker Activity ◽  
Heart Cells ◽  
Control Loop ◽  
Internal Oscillation

Rhythmic oscillations in the membrane potential of heart cells are important in normal cardiac pacemaker activity as well as cardiac arrhythmias. Two fundamentally different mechanisms of oscillatory activity can be distinguished at the cellular and subcellular level. The first mechanism, referred to as a surface membrane oscillator, can be represented by a control loop in which membrane potential changes evoke delayed conductance changes and vice versa. Since the surface membrane potential is a key variable within the control loop, the oscillation can be interrupted at any time by holding the membrane potential constant with a voltage clamp. This mode of oscillation seems to describe spontaneous pacemaker activity in the primary cardiac pacemaker (sinoatrial node) as well as other regions (Purkinje fibre, atrial or ventricular muscle). In all tissues studied so far, the pacemaker depolarization is dominated by the slow shutting-off of an outward current, largely carried by potassium ions. The second mechanism can be called an internal oscillator since it depends upon a subcellular rhythm generator which is largely independent from the surface membrane. Under voltage clamp, the existence of the internal oscillation is revealed by the presence of oscillations in membrane conductance or contractile force which occur even though the membrane potential is held fixed. The two oscillatory mechanisms are not mutually exclusive; the subcellular mechanism can be preferentially enhanced in any given cardiac cell by conditions which elevate intracellular calcium. Such conditions include digitalis intoxication, high Cao, low Nao, low or high Ko, cooling, or rapid stimulation. Several lines of evidence suggest that the subcellular mechanism involves oscillatory variations in myoplasmic calcium, probably due to cycles of Ca uptake and release by the sarcoplasmic reticulum. The detailed nature of the Cai oscillator and its interaction with the surface membrane await further investigation.

Physiological Properties of Central Medial and Central Lateral Amygdala Neurons

1999 ◽  
Vol 82 (4) ◽  
pp. 1843-1854 ◽  
Author(s):  
Marzia Martina ◽  
Sébastien Royer ◽  
Denis Paré
Keyword(s):  
Conditioned Fear ◽  
Brain Slices ◽  
Cell Types ◽  
Membrane Depolarization ◽  
Membrane Properties ◽  
Repetitive Firing ◽  
Inward Rectification ◽  
Current Pulses ◽  
Outward Rectification ◽  
Physiological Properties

Mounting evidence implicates the central (CE) nucleus of the amygdala in the mediation of classically conditioned fear responses. However, little data are available regarding the intrinsic membrane properties of CE amygdala neurons. Here, we characterized the physiological properties of CE medial (CEM) and CE lateral (CEL) amygdala neurons using whole cell recordings in brain slices maintained in vitro. Several classes of CE neurons were distinguished on the basis of their physiological properties. Most CEM cells (95%), here termed “late-firing neurons,” displayed a marked voltage- and time-dependent outward rectification in the depolarizing direction. This phenomenon was associated with a conspicuous delay between the onset of depolarizing current pulses and the first action potential. During this delay, the membrane potential ( V m) depolarized slowly, the steepness of this depolarizing ramp increasing as the prepulse V m was hyperpolarized from −60 to −90 mV. Low extracellular concentrations of 4-aminopyridine (30 μM) reversibly abolished the outward rectification and the delay to firing. Late-firing CEM neurons displayed a continuum of repetitive firing properties with cells generating single spikes at one pole and high-frequency (≥90 Hz) spike bursts at the other. In contrast, only 56% of CEL cells displayed the late-firing behavior prevalent among CEM neurons. Moreover, these CEL neurons only generated single spikes in response to membrane depolarization. A second major class of CEL cells (38%) lacked the characteristic delay to firing observed in CEM cells, generated single spikes in response to membrane depolarization, and displayed various degrees of inward rectification in the hyperpolarizing direction. In both regions of the CE nucleus, two additional cell types were encountered infrequently (≤ 6% of our samples). One type of neurons, termed “low-threshold bursting cells” had a behavior reminiscent of thalamocortical neurons. The second type of cells, called “fast-spiking cells,” generated brief action potentials at high rates with little spike frequency adaptation in response to depolarizing current pulses. These findings indicate that the CE nucleus contains several types of neurons endowed with distinct physiological properties. Moreover, these various cell types are not distributed uniformly in the medial and lateral sector of the CE nucleus. This heterogeneity parallels anatomic data indicating that these subnuclei are part of different circuits.

Ca2+-activated Cl− current in cultured myenteric neurons from murine proximal colon

2003 ◽  
Vol 284 (4) ◽  
pp. C839-C847 ◽  
Author(s):  
Sok Han Kang ◽  
Pieter Vanden Berghe ◽  
Terence K. Smith
Keyword(s):  
Membrane Potential ◽  
Channel Blocker ◽  
Reversal Potential ◽  
Outward Current ◽  
Proximal Colon ◽  
Time Dependent ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Myenteric Neurons ◽  
Whole Cell Patch Clamp

Whole cell patch-clamp recordings were made from cultured myenteric neurons taken from murine proximal colon. The micropipette contained Cs+ to remove K+ currents. Depolarization elicited a slowly activating time-dependent outward current ( I tdo), whereas repolarization was followed by a slowly deactivating tail current ( I tail). I tdo and I tail were present in ∼70% of neurons. We identified these currents as Cl− currents ( I Cl), because changing the transmembrane Cl− gradient altered the measured reversal potential ( E rev) of both I tdo and I tail with that for I tailshifted close to the calculated Cl− equilibrium potential ( E Cl). I Cl are Ca2+-activated Cl− current [ I Cl(Ca)] because they were Ca2+dependent. E Cl, which was measured from the E rev of I Cl(Ca) using a gramicidin perforated patch, was −33 mV. This value is more positive than the resting membrane potential (−56.3 ± 2.7 mV), suggesting myenteric neurons accumulate intracellular Cl−. ω-Conotoxin GIVA [0.3 μM; N-type Ca2+ channel blocker] and niflumic acid [10 μM; known I Cl(Ca) blocker], decreased the I Cl(Ca). In conclusion, these neurons have I Cl(Ca) that are activated by Ca2+entry through N-type Ca2+ channels. These currents likely regulate postspike frequency adaptation.

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