Effect of a spider toxin (JSTX) on excitatory postsynaptic current at neuromuscular synapse of spiny lobster

1. We studied the blocking properties of a spider (Nephila clavata) toxin (JSTX) purified from venom on the spiny lobster neuromuscular junction. 2. When a small amount of JSTX was applied to the neuromuscular junction, the excitatory postsynaptic potential (EPSP) was partially suppressed. The amplitude of EPSPs remained at a steady level for several hours during the washing of the preparation, showing that the action of JSTX is irreversible. 3. We recorded the excitatory postsynaptic current (EPSC) from synaptic site using a macro-patch electrode. The amplitude of EPSC increased linearly with hyperpolarization of the membrane potential in the presence and absence of JSTX. 4. The decay phase time constant of EPSC and spontaneous EPSC was decreased by hyperpolarizing the membrane potential both in the absence and in the presence of JSTX. The relationship between the decay time constant and the membrane potential was not modified by JSTX. 5. It is suggested that JSTX irreversibly blocks EPSC by acting on the site that is apart from the ionic channel of the glutamate receptor molecule.

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Desensitization onset and recovery at the potassium-depolarized frog neuromuscular junction are voltage sensitive.

The Journal of General Physiology ◽

10.1085/jgp.71.3.285 ◽

1978 ◽

Vol 71 (3) ◽

pp. 285-299 ◽

Cited By ~ 17

Author(s):

B Scubon-Mulieri ◽

R L Parsons

Keyword(s):

Membrane Potential ◽

Neuromuscular Junction ◽

Time Constant ◽

Time Course ◽

Voltage Dependence ◽

Onset Time ◽

Control Voltage ◽

Frog Neuromuscular Junction ◽

End Plate ◽

Voltage Dependent

The influence of voltage on the time-course of desensitization onset and recovery has been studied at the frog neuromuscular junction. The activation-desensitization sequence was determined from carbachol-induced end-plate currents in potassium-depolarized fibers voltage-clamped either to -40 mV or +40 mV. The time-course of both desensitization onset and recovery developed exponentially, with onset occurring more rapidly than recovery. Desensitization onset was voltage dependent, the onset time constant being 8.3 +/- 1.3 s (11 fibers) at -40 mV and 19.3 +/- 3.4 s (15 fibers) at +40 mV. Recovery from desensitization was also influenced by voltage. The extent of recovery after 2 min was 80.4 +/- 6.3% in those fibers voltage-clamped to -40 mV and 57.4 +/- 3.6% in those fibers voltage-clamped to +40 mV. The voltage dependence of desenistization onset and recovery did not result from a difference in ability to control voltage at these two levels of membrane potential. These results demonstrate that in the potassium-depolarized preparation the processes controlling both desensitization onset and recovery of sensitivity from the desensitivity from the desensitized state are influenced by membrane voltage.

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Faculty Opinions recommendation of The effect of intracellular acidification on the relationship between cell volume and membrane potential in amphibian skeletal muscle.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1020934.298840 ◽

2005 ◽

Author(s):

Martin J. Kushmerick

Keyword(s):

Skeletal Muscle ◽

Membrane Potential ◽

Cell Volume ◽

Intracellular Acidification ◽

The Relationship

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Effect of low chloride on relaxation in hamster diaphragm muscle

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.1.180 ◽

1986 ◽

Vol 61 (1) ◽

pp. 180-184 ◽

Cited By ~ 11

Author(s):

S. A. Esau ◽

N. Sperelakis

Keyword(s):

Membrane Potential ◽

Muscle Fatigue ◽

Time Constant ◽

Diaphragm Muscle ◽

Resting Membrane Potential ◽

Krebs Solution ◽

Sarcolemmal Membrane ◽

Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

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Computer Simulation of the Responses of Human Motoneurons to Composite 1A EPSPS: Effects of Background Firing Rate

Journal of Neurophysiology ◽

10.1152/jn.1997.77.1.405 ◽

1997 ◽

Vol 77 (1) ◽

pp. 405-420 ◽

Cited By ~ 36

Author(s):

Kelvin E. Jones ◽

Parveen Bawa

Keyword(s):

Computer Simulation ◽

Firing Rate ◽

Time Course ◽

Current Model ◽

Response Probability ◽

Muscle Spindles ◽

Excitatory Postsynaptic Potential ◽

Biophysical Properties ◽

Rhythmic Firing ◽

The Relationship

Jones, Kelvin E. and Parveen Bawa. Computer simulation of the responses of human motoneurons to composite 1A EPSPS: effects of background firing rate. J. Neurophysiol. 77: 405–420, 1997. Two compartmental models of spinal alpha motoneurons were constructed to explore the relationship between background firing rate and response to an excitatory input. The results of these simulations were compared with previous results obtained from human motoneurons and discussed in relation to the current model for repetitively firing human motoneurons. The morphologies and cable parameters of the models were based on two type-identified cat motoneurons previously reported in the literature. Each model included five voltage-dependent channels that were modeled using Hodgkin-Huxley formalism. These included fast Na+ and K+ channels in the initial segment and fast Na+ and K+ channels as well as a slow K+ channel in the soma compartment. The density and rate factors for the slow K+ channel were varied until the models could reproduce single spike AHP parameters for type-identified motoneurons in the cat. Excitatory synaptic conductances were distributed along the equivalent dendrites with the same density described for la synapses from muscle spindles to type-identified cat motoneurons. Simultaneous activation of all synapses on the dendrite resulted in a large compound excitatory postsynaptic potential (EPSP). Brief depolarizing pulses injected into a compartment of the equivalent dendrite resulted in pulse potentials (PPs), which resembled the compound EPSPs. The effects of compound EPSPs and PPs on firing probability of the two motoneuron models were examined during rhythmic firing. Peristimulus time histograms, constructed between the stimulus and the spikes of the model motoneuron, showed excitatory peaks whose integrated time course approximated the time course of the underlying EPSP or PP as has been shown in cat motoneurons. The excitatory peaks were quantified in terms of response probability, and the relationship between background firing rate and response probability was explored. As in real human motoneurons, the models exhibited an inverse relationship between response probability and background firing rate. The biophysical properties responsible for the relationship between response probability and firing rate included the shapes of the membrane voltage trajectories between spikes and nonlinear changes in PP amplitude during the interspike interval at different firing rates. The results from these simulations suggest that the relationship between response probability and background firing rate is an intrinsic feature of motoneurons. The similarity of the results from the models, which were based on the properties of cat motoneurons, and those from human motoneurons suggests that the biophysical properties governing rhythmic firing in human motoneurons are similar to those of the cat.

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Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-284 ◽

1987 ◽

Vol 65 (9) ◽

pp. 1821-1831 ◽

Cited By ~ 4

Author(s):

E. Honoré ◽

M. M. Adamantidis ◽

B. A. Dupuis ◽

C. E. Challice ◽

P. Guilbault

Keyword(s):

Membrane Potential ◽

Guinea Pig ◽

Papillary Muscle ◽

Cardiac Cells ◽

Resting Membrane Potential ◽

Tonic Component ◽

Contraction Coupling ◽

Rich Solution ◽

The Relationship ◽

Guinea Pig Atria

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 μM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.

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Respiratory mechanics in mechanically ventilated patients with respiratory failure

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.6.1849 ◽

1985 ◽

Vol 58 (6) ◽

pp. 1849-1858 ◽

Cited By ~ 141

Author(s):

A. Rossi ◽

S. B. Gottfried ◽

B. D. Higgs ◽

L. Zocchi ◽

A. Grassino ◽

...

Keyword(s):

Time Constant ◽

Inflation Rate ◽

Respiratory Mechanics ◽

Mechanically Ventilated ◽

Mechanically Ventilated Patients ◽

Airway Occlusion ◽

The Relationship ◽

Resistance Value ◽

Ventilated Patients

In 11 mechanically ventilated patients, respiratory mechanics were measured 1) during constant flow inflation and 2) following end-inflation airway occlusion, as proposed in model analysis (J. Appl. Physiol. 58: 1840–1848, 1985. During the latter part of inflation, the relationship between driving pressure and lung volume change was linear, allowing determination of static respiratory elastance (Ers) and resistance (RT). The latter represents in each patient the maximum resistance value that can obtain with the prevailing time constant inhomogeneity. Following occlusion, Ers and RT were also obtained along with RT (min) which represents a minimum, i.e., resistance value that would obtain in the absence of time constant inhomogeneity. A discrepancy between inflation and occlusion Ers and RT was found only in the three patients without positive end-expiratory pressure, and could be attributed to recruitment of lung units during inflation. In all instances Ers and RT were higher than normal. RT(min) was lower in all patients than the corresponding values of RT, indicating that resistance was frequency dependent due to time constant inequalities. Changes in inflation rate did not affect Ers, while RT increased with increasing flow.

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Chloride Accumulation as a Homeostatic System: Negative Feedback Signals for Concentration and Turgor Maintenance Differ in a Glycophyte and a Halophyte

Functional Plant Biology ◽

10.1071/pp9800237 ◽

1980 ◽

Vol 7 (3) ◽

pp. 237 ◽

Cited By ~ 11

Author(s):

WJ Cram

Keyword(s):

Negative Feedback ◽

Turgor Maintenance ◽

Non Linear ◽

Steady Level ◽

Homeostatic System ◽

Chloride Accumulation ◽

Relationship Of ◽

The Relationship ◽

Uptake Of Nutrients

Carrot tissue is taken as a representative glycophilic tissue. It accumulates K+, Cl- and total osmotica to a steady level after 10-15 days. This level of Cl- is nearly constant and is independent of external KCl concentration and of turgor. Cl- influx is also independent of turgor. It therefore appears that the Cl- accumulating system in carrot (and possibly in other glycophytes) can, under artificial conditions, act as a homeostat for intracellular C- concentration, and is not the basis of turgor maintenance. It is suggested that turgor might be maintained by controlled accumulation of K+ carboxylates in glycophytes. Beet tissue is taken as a representative halophilic tissue. It accumulates K+, Cl-, and total osmotica to a steady level after about 4 days. At this stage turgor is constant, due to differences in the levels of KCl accumulated. Cl- influx is stimulated by reducing turgor after a lag of 3-5 h. The relationship of Cl- influx to turgor is non-linear. It therefore appears that in beet (and possibly in other halophytes) turgor maintenance is based on the turgor-sensitive accumulation of Cl- salts. Cl- influx in beet is also affected by changes in intracellular Cl- concentration, as in carrot. It is suggested that this feedback relationship may primarily be part of a system for the controlled uptake of nutrients rather than of Cl- in both tissues.

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

Journal of Neurophysiology ◽

10.1152/jn.1988.59.5.1352 ◽

1988 ◽

Vol 59 (5) ◽

pp. 1352-1376 ◽

Cited By ~ 78

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)

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Investigating two kinds of cellular alternans and corresponding TWA induced by impaired calcium cycling in myocardial ischemia

Mathematical Biosciences and Engineering ◽

10.3934/mbe.2021379 ◽

2021 ◽

Vol 18 (6) ◽

pp. 7648-7665

Author(s):

Jiaqi Liu ◽

◽

Zhenyin Fu ◽

Yinglan Gong ◽

Ling Xia

Keyword(s):

Myocardial Ischemia ◽

Conduction Velocity ◽

Ionic Channel ◽

Calcium Cycling ◽

One Dimensional ◽

T Wave ◽

Cell Simulation ◽

T Wave Alternans ◽

Dimensional Simulation ◽

The Relationship

<abstract> <sec><title>Background</title>The utility of T wave alternans (TWA) in identifying arrhythmia risk has been demonstrated. During myocardial ischemia (MI), TWA could be induced by cellular alternans. However, the relationship between cellular alternans patterns and TWA patterns in MI has not been investigated thoroughly. </sec> <sec><title>Methods</title>We set MI conditions to simulate alternans. Either prolonging Ca2+ release or increasing spark-induced sparks (secondary sparks) can give rise to different patterns of APD alternans and TWA. In addition, different ischemic zones and reduced conduction velocity are also considered in one dimensional simulation. </sec> <sec><title>Results</title>Delay of Ca2+ release can produce discordant Ca2+-driven alternans in single cell simulation. Increasing secondary sparks leads to concordant alternans. Correspondingly, morphology and magnitude of TWA vary in two different cellular alternans. Epi ischemia results in alternans concentrating in the first half of T wave. Endo and transmural ischemia lead to fluctuations in the second half of T wave. In addition, slowing conduction velocity has no effect on TWA magnitude. </sec> <sec><title>Conclusion</title>Specific ionic channel dysfunction and ischemic zones affect TWA patterns. </sec> </abstract>

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