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PubMed1974

On facilitation of transmitter release at the toad neuromuscular junction.

1. The time dependence of the increase in amplitude (facilitation) of a second end-plate potential (e.p.p.) elicited within 10-100 msec of a preceding e.p.p. was examined at neuromuscular junctions in sartorius muscles of toads. Facilitation was defined by two characteristics, initial facilitation and the time constant of its exponential decay.2. The time constant of decay of facilitation was longer at lower temperatures and the Q(10) was 4.3 in the range 10-25 degrees C. There was no significant effect of temperature on initial facilitation.3. Ouabain (10(-4)-10(-3)M), lithium substitution for sodium, sodium azide (5 mM) and N-ethylmaleimide (NEM, 0.1 mM) initially had no effect on initial facilitation or the decay of facilitation. After some time, they all caused a longer time constant of decay of facilitation and a depression of initial facilitation.4. It was concluded that the decay of facilitation is not directly dependent on active transport of sodium ions, calcium efflux, ATP-dependent movements of calcium or mitochondrial uptake of calcium following an action potential.5. Ouabain, lithium, sodium azide, and NEM all caused an increase in transmitter release. This effect, and the late effects on facilitation, were thought to be due to an increase in intracellular calcium concentration in nerve terminals.6. No relationship was found between the quantal content of e.p.p.s (range, 0.8-100) and initial facilitation, or the time constant of decay of facilitation.7. Substitution of strontium for calcium ions caused a marked prolongation of the time constant of decay of facilitation, and a depression of initial facilitation.8. The results were consistent with the hypothesis that the time constant of decay of facilitation is related to the rate of disappearance of an ;active' complex of calcium (CaA) which, of itself, is not sufficient for transmitter release. It is suggested that an action potential produces CaA which decays with the time constant of facilitation and CaS, a short-life complex of calcium which decays with the time constant of the phasic release of transmitter. The release of transmitter is proportional to some function of [CaA] and [CaS].

Action Potentials↗
PubMed1975

The effect of procaine on the action of acetylcholine at the neuromuscular junction.

1. The effect of procaine on acetylcholine-induced membrane fluctuations (ACh noise) was studied by intracellular and focal external recording from end-plates of frog sartorius muscle. 2. With intracellular recording, ACh noise (the ratio of variance to mean depolarization) was substantially reduced by procaine, suggesting a greatly decreased amplitude of the elementary potential change. 3. Spectral analysis of the ACh noise indicated a dual average time course of the underlying "shot effects", similar to the complex shape (brief spike followed by a long tail of low intensity) of the end-plate current in pro-aine-treated muscle. 4. The post-synaptic blocking action of procaine can be largely explained by the drastic shortening of the initial high-intensity phase of the end-plate conductance change. 5. The average time course of the ACh shot effects is discussed in terms of alternative hypotheses, one attributing the complex shape to each elementary event, the other involving sequential reaction steps which produce two unequal populations of ion gates of different "life-times".

Acetylcholine↗
PubMed1976

The voltage dependence of membrane capacity.

1. Membrane capacity of sartorius muscle fibres has been measured at membrane potentials between -200 and +50 mV. Within this potential range the capacity is not independent of potential. Dielectric saturation is present at large negative and at positive internal potentials, indicating the presence in the membrane of permanent dipoles or movable charges. 2. In normally polarized fibres there is a sharp peak in the capacity-potential relation of about -50 mV; the capacity at this peak is 50% larger than the capacity at -90 mV. 3. In depolarized fibres this sharp peak of capacity is not present. Over the range -200 to +50 mV the capacity variation is about 10% with a broad maximum at about -80 mV. 4. The dielectric behaviour of muscle membrane is most simply explained by postulating two species of permanent dipoles or mobile charges: Charge 1 present in normally polarized fibres, but neutralized or immobilized in depolarized fibres; Charge 2 present in both polarized and depolarized fibres. The distribution of Charge 1 is more steeply voltage-dependent than is the distribution of Charge 2. 5. Movement of Charge 1 from one fully saturated configuration to the other involves a charge transfer across the membrane of between 20 and 30 nC/muF. Movement of Charge 2 in depolarized fibres requires a similar transfer of charge.

Animals↗
PubMed1976

Relationship between initial chemical reactions and oxidative recovery metabolism for single isometric contractions of frog sartorius at 0 degrees C.

1. Measurements of intitial chemical changes and recovery oxygen consumption (deltaO2) were made in unpoisoned aerobic frog sartorius muscles at 0 degrees C to provide independent measures of the chemical energy used for isometric tetani of various durations. 2. DeltaO2 was measured polarographically and increased in a curvilinear fashion with stimulus duration. For stimulations longer than 4 sec deltaO2 was a linear function of the tension-time integral. 3. Measurements of the changes in the content of phosphorylcreatine, 'free' creatine and inorganic phosphate were made in muscles rapidly frozen during a tetanus. The average of these quantities, delta approximately P, was used to measure the initial 'high energy' phosphate utilization. No break-down of 'high-energy' phosphate compounds was detected up to 200 sec after relaxation of tension. Changes in the content of ATP were not observed except for a small decrease (-0-25+/-0-1 mumole/g) in muscles tetanized for 1 sec. 4. Delta approximately P also increase curvilinearly with tetanus duration and, for tetanic durations greater than 4 sec, was a linear function of the tension-time integral. 5. Both deltaO2 and delta approximately P were quantitatively related by a constant scaling factor of about 4-3 (delta approximately P/deltaO2) throughout the range of tetanic durations studied. The constancy of this ratio.provides evidence against the hypothesis that a significant 'missing reaction' provides energy during any one portion of the tetanus. Several hypothesis may account for the numerical value of the ration delta approximately P/deltaO2.

Adenosine Triphosphate↗
PubMed1978

Octanol reduces end-plate channel lifetime.

1. Post-synaptic effects of n-octanol at concentrations of 0.1-1 mM were examined in toad sartorius muscles by use of extracellular and voltage-clamp techniques.2. Octanol depressed the amplitude and duration of miniature end-plate currents and hence depressed neuromuscular transmission.3. The decay of miniature end-plate currents remained exponential in octanol solutions even when the time constant of decay (tau(D)) was decreased by 80-90%.4. The lifetime of end-plate channels, obtained by analysis of acetylcholine noise, was also decreased by octanol. The average lifetime measured from noise spectra agreed reasonably well with the time constant of decay of miniature end-plate currents, both in control solution and in octanol solutions.5. Octanol caused a reduction in the conductance of end-plate channels. Single channel conductance was on average about 25 pS in control solution and 20 pS in octanol.6. In most cells the normal voltage sensitivity of the decay of miniature end-plate currents was retained in octanol solutions. The lifetime of end-plate channels measured from acetylcholine noise also remained voltage-sensitive in octanol solutions. In some experiments in which channel lifetime was exceptionally reduced the voltage sensitivity was less than normal.7. In octanol solutions, tau(D) was still very sensitive to temperature changes in most cells although in some the temperature sensitivity of tau(D) was clearly reduced. Changes in tau(D) with temperature could generally be fitted by the Arrhenius equation suggesting that a single step reaction controlled the decay of currents both in control and in octanol solutions. In some cells in which tau(D) became less than 0.3 ms, the relationship between tau(D) and temperature became inconsistent with the Arrhenius equation.8. As the decay of end-plate currents in octanol solutions remains exponential, and the voltage and temperature sensitivity can be unchanged even when tau(D) is significantly reduced, it seems likely that octanol decreases tau(D) by increasing the rate of the reaction which normally controls the lifetime of end-plate channels.

Animals↗
PubMed1979

Dual effects of ether on end-plate currents.

1. The effects of diethyl ether (ether) on miniature end-plate currents (m.e.p.c.s) and on acetylcholine-activated end-plate channels were measured in toad sartorius muscle fibres with voltage-clamp and extracellular recording techniques. 2. At low concentrations (less than 20 mM) either made m.e.p.c.s decay faster than normal. At high concentrations (greaster than 40 mM), the decay of m.e.p.c.s was slower than normal. With all concentrations, the cecay remained exponential with single time constant, tau D. 3. At low concentrations ether did not affect the growth phase of m.e.p.c.s and only slightly reduced the amplitude of m.e.p.c.s. At the higher concentrations, the growth phase was slowed and m.e.p.c.s were significantly reduced in amplitude. 4. Ether at all concentrations (5--70 mM) reduced end-plate channel lifetime, the effect increasing with ether concentration. Ether did not significantly alter the elementary channel conductance or the actylcholine null (reversal) potential. 5. Curare reduced tau D which had been prolonged by high concentrations of ether. Ether itself at high concentrations caused a reduction in tau D increased by neostigmine. It is proposed that high concentrations of either inhibit acetylcholine hydrolysis by acetylcholinesterase. 6. The effect of ether in reducing end-plate channel lifetime and reducing m.e.p.c. amplitude, without significantly altering the normal voltage and temperature sensitivity of channel lifetime, is consistent with the proposal that either reduces the stability of open end-plate channels.

Acetylcholine↗
PubMed1983

Electrophysiological and chemical determination of acetylcholine release at the frog neuromuscular junction.

1. Mass fragmentography was used to measure the tissue content and release of acetylcholine (ACh) by frog sartorius muscles, which had been previously treated with an irreversible cholinesterase inhibitor. The frequency of miniature end-plate currents (m.e.p.c.s) was also measured. 2. Exposure of muscles for 15 min to 2 mM-LaCl3 resulted in a large release of ACh which subsided to low levels after 1 h. About 4 h later treatment with 50 mM-KCl, or with the calcium ionophore A 23187, or with a second dose of LaCl3, all failed to augment ACh release, notwithstanding the fact that the ACh content of La3+-treated muscles was about the same as that of controls. 3. Hypertonic NaCl or raised KCl concentrations were used to increase m.e.p.c.s and this also increased ACh release; it was estimated that each quantum corresponded to the release of 12 000 molecules of ACh. 4. ACh release by nerve stimulation was greatly potentiated by 10 mM-tetraethylammonium chloride, and this enabled the ACh released by ten, and even single, stimuli to be detected; it was calculated from the ACh released and the quantal content that each quantum contained on the average 13 000 molecules. 5. ACh released by nerve stimulation at 0.2/s in the absence of tetraethylammonium was about half that expected on the basis of previous estimates of quantal content; it was increased about two-fold by alpha-bungarotoxin. 6. It is concluded that chemical and electrical stimulation of the nerve evoked quantal ACh release, without influencing non-quantal ACh leakage. The results are consistent with the view that ACh quanta are derived from synaptic vesicles. They also show that resting ACh release is not due to leakage of ACh ions along an electrochemical gradient in the membrane.

Acetylcholine↗
PubMed1983

Sites of action of procaine at the motor end-plate.

The effects of procaine at pH 7.4 and 9.9 were studied by examining the decay phase of spontaneous miniature end-plate currents (m.e.p.c.s) recorded from toad sartorius muscle fibres. Following exposure to procaine (0.05-0.1 mM) at pH 7.4, the decay of m.e.p.c.s rapidly became biphasic, and could be described as the sum of two exponential components. When the same concentrations of procaine were applied at pH 9.9, the development of biphasic m.e.p.c.s took much longer. Reversal of the effect upon washing out the procaine was much slower at pH 9.9 than at pH 7.4. A rapid change in pH from 7.4 to 9.9 during exposure to a constant concentration of procaine quickly reduced the effect of procaine on m.e.p.c.s. The effect gradually returned after prolonged exposure to procaine at pH 9.9. These results suggest that procaine applied at high pH, where it is predominantly in uncharged form, may be diffusing to a site of action which is not directly accessible from the external surface of the membrane. The voltage-dependence of procaine action was similar whether it was applied at pH 7.4 or 9.9. Intracellular injection of procaine rapidly produced biphasic m.e.p.c.s, whether the extracellular pH was 7.4 or 9.9. The effect of membrane potential on these m.e.p.c.s was similar to that seen for biphasic m.e.p.c.s produced by extracellular application of procaine. The results indicate that procaine can affect end-plate channels when applied to either surface of the muscle membrane, and that the voltage-dependence of procaine action does not arise from the influence of membrane field on the movement of charged procaine molecules into open channels.

Animals↗
PubMed1983

The calcium dependence of spontaneous and evoked quantal release at the frog neuromuscular junction.

1. The quantal output from stimulated nerve terminals in the frog sciatic nerve-sartorius muscle preparation in low-Ca(2+) Ringer solution was measured by the coefficient of variation and the failures methods. Adding sucrose to the Ringer to increase the tonicity or adding ethanol increased miniature end-plate potential (m.e.p.p.) frequency and also the end-plate potential (e.p.p.) amplitude. Earlier reports suggested that increases in tonicity did not increase evoked quantal release.2. Concanavalin A has been reported to block the increase in m.e.p.p. frequency caused by increasing the tonicity of the Ringer (Gorio & Mauro, 1979). This effect was confirmed. The lectin-treated preparations also failed to show an increase in evoked quantal release when the tonicity was increased.3. A model in which both spontaneous and evoked quantal releases depend on some power of the intracellular [Ca(2+)] is presented. The model predicts that rises in m.e.p.p. frequency will be accompanied by increased quantal output from stimulated nerve terminals. The maximum slope of the relationship between log (evoked quantal output) and log ([Ca(2+)](out)) will be less than the true power. A theoretical analysis shows that, as the true power approaches infinity, the maximum slope will be slightly above 4. The value for the slope usually found experimentally at the frog neuromuscular junction is also about 4.4. The model does not fit the experimental data. The observed increases in evoked quantal release are higher than those predicted for the observed increases in spontaneous release. There are several possible explanations for the discrepancy. Treatments that increase m.e.p.p. frequency may also increase Ca(2+) influx into the stimulated terminal. However, we prefer the explanation that there is a fraction of spontaneous release that is independent of the [Ca(2+)] in the terminal; if this is true the model might account for the data.5. The model can account for a variety of puzzling experimental observations, including: (a) the effect of hypertonic solutions and of diamine in decreasing the slope in the relation between log (evoked quantal output) and log ([Ca(2+)](out)); (b) the slope of near 1 observed at the crustacean neuromuscular junction; (c) the decrease in the slope produced by treatment with botulinum toxin.

Action Potentials↗
PubMed1984

Some effects of procaine at the toad end-plate are not consistent with a simple channel-blocking model.

Miniature end-plate currents (m.e.p.c.s) were recorded extracellularly from toad sartorius muscle fibres exposed to solutions containing procaine at pH 5.4, 7.4 and 9.9. The decay phase of m.e.p.c.s was analysed to determine whether the effects of procaine were consistent with a sequential channel-blocking model. Averaged m.e.p.c.s measured in the presence of procaine were biphasic, decaying as the sum of two exponential components. However, about 10-15% of m.e.p.c.s decayed as single exponentials and were not biphasic. At pH 9.9 the relative amplitudes of the fast and slow phases were generally consistent with the decay time constants, according to the predictions of the blocking model. Such a correlation was not found at pH 5.4 or 7.4. In addition, the rate of decay of m.e.p.c.s at pH 5.4 did not increase as predicted with procaine concentration. These results demonstrate that the sequential blocking model is unable to account for all of the effects of procaine on m.e.p.c. decay. In addition, the finding that some m.e.p.c.s are single exponentials, while most are biphasic, suggests a heterogeneity of receptor-channel complexes.

Animals↗
PubMed1986

Estimating the time course of evoked quantal release at the frog neuromuscular junction using end-plate current latencies.

The use of end-plate current (e.p.c.) latency measurements to estimate the time course of the stochastic probabilistic process governing evoked release was investigated in the sciatic nerve-sartorius muscle preparation of the frog, Rana pipiens. We also examined the possibility that the release of a quantum depresses or enhances the subsequent release of additional quanta. Muscle end-plates were voltage clamped at 3-4 degrees C. Quantal release was restricted to a short, or localized, region of the nerve terminal using Ca2+-free, EGTA Ringer solution and a Ca2+-filled micropipette. The number of e.p.c.s containing 0, 1, 2, etc. quanta were totalled and compared to numbers predicted using Poisson's theorem. The differences between the actual and predicted numbers of events were not significant at the nineteen junctions studied (P less than 0.05). The latency of the first quantum observed in several hundred e.p.c.s was measured and used to calculate an estimate, alpha 1(t), of the time-dependent, probabilistic process, alpha (t), governing all evoked quantal release (Barrett & Stevens, 1972b). In three experiments, all quantal latencies were measured to obtain the actual alpha (t). The alpha 1(t) function gave an excellent approximation of alpha (t) (P greater than 0.2), in real and simulated latency data. The latency of the second quantum in the e.p.c.s was measured and used to provide another estimate, alpha 2(t), of alpha (t). The alpha 2(t) function was lower (depressed) during the first few milliseconds of the evoked release period, relative to alpha 1(t). The difference was significant (P greater than 0.01) in all experiments. Our measurement procedures were tested using computer-generated 'e.p.c.s' containing randomly occurring 'quanta'. These tests showed that the early depression was due to inadequate detection of the second quantum in the e.p.c.s. The effect of Sr2+ on evoked release was examined using double-barrelled pipettes containing 1 M-SrCl2 and CaCl2 solutions. The major result was that the durations of alpha 1(t) and alpha 2(t) were equally lengthened in Sr2+, relative to Ca2+.

Animals↗
PubMed1987

Effect of chloride ions on giant miniature end-plate potentials at the frog neuromuscular junction.

1. Frog sartorius muscles were incubated in Ringer solutions with a raised K+ concentration (high K+) and then allowed to recover in medium with a normal K+ concentration. During the recovery period miniature end-plate potentials (m.e.p.p.s) were recorded with intracellular electrodes. In addition, the acetylcholine (ACh) released from muscles in the presence of high K+ was measured by a mass spectrometric method. 2. Incubation in a high-K+ medium induced the appearance of giant miniature end-plate potentials (g.m.e.p.p.s). However, if the Cl- of the medium was substituted by propionate, very few g.m.e.p.p.s were observed. This was due to the absence of Cl- and not to the presence of propionate. The frequency of g.m.e.p.p.s was also greatly depressed when the Cl- concentration was lowered from 120 to 60 mM. 3. The amount of ACh released into a high-K+ medium was the same, regardless of whether Cl- or propionate was the anion. 4. When Cl- was replaced by NO3- or Br-, incubation in high-K+ Ringer solution induced the appearance of g.m.e.p.p.s. However, SO4(2-), like propionate, was unable to substitute for Cl- in this respect. 5. The frequency of g.m.e.p.p.s was correlated with that of m.e.p.p.s during the recovery period. However, when the K+ concentration was raised to 17 mM the frequency of m.e.p.p.s greatly increased, whereas that of the g.m.e.p.p.s did not change significantly. 6. G.m.e.p.p.s disappeared in the presence of curare, but persisted in the presence of tetrodotoxin or in a Ca2+-lacking medium. However, g.m.e.p.p.s failed to appear when the medium had lacked Ca2+ during the stimulation. 7. It is tentatively concluded that g.m.e.p.p.s are associated with Cl--dependent processes which occur after stimulation of transmitter release, and which are linked with the endocytotic retrieval of presynaptic membrane.

Acetylcholine↗
PubMed1989

Factors affecting aerobic recovery heat production and recovery ratio of frog sartorius.

1. Sartorius muscles of Rana temporaria, equilibrated at 20 degrees C in Ringer solution buffered with phosphates, were stimulated isometrically for 0.2 up to 0.75 s at lengths varying from 1.03 to 1.48 times rest length, L0. The aerobic recovery heat was measured for 10.5 min after contraction. 2. The recovery heat production had a complex time course, showing a variable delay to maximum, declining thereafter. In most cases, the rate of heat production did not decrease monotonically; attention was focused on the slow exponential decay which only persisted from 1.5-5 min after contraction. This latter part of the time course was considered as strictly aerobic and characterized by the time constant tau s. 3. Increasing the tetanus duration from 0.2 to 0.75 s increased initial heat Qi and recovery heat Qr in proportion, so that the recovery ratio R (Qr/Qi) did not change; it was equal to 1.29 +/- 0.03 (S.E.M.; n = 44) for muscles at about L0. The kinetics of heat production were modified with longer tetani; in particular, tau s was increased from 2.2 to 5.2 min. 4. When muscles were stretched beyond L0, as long as there was no increase of the resting heat rate (stretch response or 'Feng effect'), recovery heat production had a similar evolution to that in muscles at about L0; R was constant and equal to 1.21 +/- 0.03 (n = 46). 5. When muscles were sufficiently stretched to develop a stretch response, R increased proportionally to the stretch response. The effect seemed independent of the contractile machinery, as it vanished concomitantly with the stretch response, while force and Qi remained unchanged for the length considered. The kinetics were also modified--the delay to maximum was no longer detected and tau s most likely increased. 6. Substitution of 60% of the NaCl of the Ringer solution by NaI (mol/mol) produced a significant increase of R, mainly due to the increase of Qr. 7. The results show that neither the time course nor the amount of aerobic recovery heat Qr are strictly determined by the amount of initial heat Qi. The hypothesis is discussed that Qr might include a variable fraction due to processes which are not directly implicated in the actin-myosin interactions, possibly those involving the cytosolic Ca2+ concentration and the rate of resting metabolism.

Animals↗
PubMed1971

Kinetics of acetylcholine synthesis and hydrolysis in myasthenia gravis.

Kinetic studies for choline-O-acetyltransferase (CAT) (E.C. 2.3.1.6) and acetylcholinesterase (E.C. 3.1.1.7) were performed on serum, skin fibroblasts in culture, and biopsied sartorius muscle from normal and myasthenic subjects. There was a significant decrease of CAT activity per milligram of protein in myasthenic muscle compared to normal muscle, and there was no difference in acetylcholinesterase activity per milligram of protein in the same muscle homogenates. Substrate concentration curves for acetyl coenzyme A and CAT also showed a significant reduction in the maximum rate of product formation (V(max)) per milligram of protein between myasthenic and normal muscle. It is postulated that binding of substrate to CAT is being inhibited by an inhibitor present in muscle.

Acetylcholine↗
PubMed1973

Diisopropylfluorophosphate: suppression of ionic conductance of the cholinergic receptor.

When frog sartorius muscles were exposed to diisopropylfluorophosphate, the amplitude and half-decay time of the end-plate current decreased; the half-decay time became almost potential-independent and the equilibrium potential for the end-plate current was more negative than during control conditions. When the excess reagent was removed by washing so that only the phosphorylated acetylcholinesterase remained, the amplitude of the end-plate current was restored, while its half-decay time was markedly increased. These findings reveal that this organophosphate significantly affects the receptor-ionic conductance modulator complex in addition to its well-known anticholinesterase activity.

Animals↗
PubMed1982

Possible role of the transverse tubules in accumulating calcium released from the terminal cisternae by stimulation and drugs.

The size of the rapidly exchanging and slowly exchanging Ca2+ pools were estimated in frog sartorius muscles. A new technique using Sr2+ to extract the rapidly exchanging pool was used. The method avoids problems of kinetic analysis. The results showed that stimulation causes Ca2+ to be translocated from a compartment which exchanges with a time constant of 800 min to a compartment that can be washed out in 15 min. This is likely a transfer from the terminal cisternae to the transverse tubule. Calculations show that this would represent 0.9% of the Ca2+ released in each twitch. After 300 twitches produced by a 1-Hz stimulation, this accumulation could have increased the Ca concentration in the transverse tubules to 70 mM. A marked increase of Ca2+ concentration of this magnitude in the transverse tubules would raise the mechanical threshold for excitation--contraction coupling and would decrease the efficiency of coupling between contraction and excitation. This could be the explanation of the fatigue observed during this kind of stimulation.

Animals↗
PubMed1993

Simple, inexpensive suction electrode system for the student physiology laboratory.

A versatile, inexpensive, easily constructed suction electrode system is described that can be used for routine exercises by the student on, or for demonstrations of, the electrophysiology of frog sciatic nerve and gastrocnemius and sartorius muscles. A disposable plastic syringe and a disposable pipette with Ag-AgCl wire comprise the suction electrode. Six readily manipulable electrodes are installed in the walls of the Plexiglas preparation bath, and an arbitrary number of additional "free" electrodes can be placed where desired. An optional small chamber, formed from a disposable plastic culture dish and Gootch rubber tubing, provides for "barrier" recording within the larger chamber. Interpretations are given of the electrical responses of nerve and muscle in terms of longitudinal currents along the preparation within the suction electrode tubes.

Animals↗
PubMed1995

Resting membrane potentials: a student test of alternate hypotheses.

The frog sartorius muscle is a model tissue for demonstrating to physiology students the principles underlying both membrane phenomena and hypothesis testing. Myocytes can be impaled with conventional glass microelectrodes to measure membrane voltage (Vm). Further, Vm is observed as extracellular K+ is altered and a K+ channel blocker is added. After the experiment, students examine the underlying assumptions of the Nernst equilibrium and the Goldman-Hodgkin-Katz equation. They ultimately determine which of the two algorithms best predicts the measured Vm. In addition, students learn micromanipulation and impalement techniques. This experiment facilitates the student's understanding of membrane permeability, ionic gradients, and membrane voltage.

Algorithms↗