Decay Of Miniature Endplate Currents Research Articles

Different sensitivity of miniature endplate currents in rat external and internal intercostal muscles to the acetylcholinesterase inhibitor C-547 as compared with diaphragm and extensor digitorum longus

Derivative of 6-methyluracil, selective cholinesterase inhibitor C-547 potentiates miniature endplate currents (MEPCs) in rat external intercostal muscles (external ICM) more effectively than in internal intercostal muscles (internal ICM). Effect of the C-547 on intercostal muscles was compared with those on extensor digitorum longus (EDL) and diaphragm muscles. Half-effective concentrations for tau of MEPC decay arranged in increasing order were as follows: EDL, locomotor muscle, most sensitive = 1.3 nM, external ICM, inspiration muscle = 6.8 nM, diaphragm, main inspiration muscle = 28 nM, internal ICM, expiration muscle = 71 nM. External ICM might therefore be inhibited, similarly as the limb muscles, by nanomolar concentrations of the drug and do not participate in inspiration in the presence of the C-547. Moreover, internal ICM inhibition can hinder the expiration during exercise-induced fast breathing of C-547- treated experimental animals.

Dependence of miniature endplate current on kinetic parameters of acetylcholine receptors activation: a model study.

Mathematical modeling was applied to study the dependence of miniature endplate current (MEPC) amplitude and temporal parameters on the values of the rate constants of acetylcholine binding to receptors (k+) when cholinesterase was either active or inactive. The simulation was performed under two different sets of parameters describing acetylcholine receptor activation--one with high and another with low probability (Pohigh and Polow) of receptor transition into the open state after double ligand binding. The dependence of model MEPC amplitudes, rise times, and decay times on k+ differs for set Polow and set Pohigh. The main outcome is that for set Pohigh, the rise time is significantly longer at low values of k+ because of the prolongation of ACh diffusion time to the receptor. For the set Polow, the rise time is shorter at low values of k+, which can be explained by the small probability of AChR forward isomerization after ACh binding and faster MEPC's peak formation.

Linalool modifies the nicotinic receptor–ion channel kinetics at the mouse neuromuscular junction

Linalool is a monoterpene compound reported to be a major component of essential oils in various aromatic species. Several linalool-producing species are used in traditional medical systems. Among these is Aeolanthus suaveolens G. Dom (Labiatae) which is used as an anticonvulsant in the Brazilian Amazon. Psychopharmacologicalin vivo evaluation of linalool showed that this compound has dose-dependent marked sedative effects at the central nervous system (CNS), including hypnotic, anticonvulsant and hypothermic properties. It has been suggested that these neurochemical effects might be ascribed to the local anaesthetic activity of linalool. The present study reports an inhibitory effect of linalool on the acetylcholine (ACh) release and on the channel open time in the mouse neuromuscular junction. These findings could provide a rational basis to confirm the traditional medical use of linalool-producing plant species. Indeed, our data demonstrate some interactions in the modulation of the ACh release at the mouse neuromuscular junction, which are well correlated with the suggested molecular mechanisms. Linalool induced a reduction of the ACh-evoked release. The possibility that this effect could be ascribed to some interaction with pre-synaptic function is noteworthy. Moreover, the inhibitory effect induced on the kinetics of the miniature end-plate current decay demonstrates a local anaesthetic action, either on the voltage or on the receptor-activated channels.

Miniature endplate current kinetics at the mouse neuromuscular junction: effects of temperature and medium viscosity.

The time course of miniature endplate currents (MEPCs), derived by extracellular focal recording, was studied in the mouse neuromuscular junction at different temperatures and medium viscosities, and in eserine-treated endplates. At low temperatures (6-10 degrees C), almost the whole MEPC decay is exponential and the rising phase is not significantly modified by the channel closing process. At physiological temperatures (38-40 degrees C), the early part of the decay is much slower than the later part and the rising phase is made shorter and smaller by channel closing, showing that the channel opening and channel closing processes overlap remarkably. Even at physiological temperatures, however, the late part of the MEPC decay shows an exponential time course. At high temperatures the channel opening process has low temperature sensitivity and slows down when bath solution viscosity is increased, suggesting that at high temperatures channel opening kinetics may mainly be controlled by the time course of acetylcholine diffusion. The lower limit of conformational change rate leading to channel opening was estimated at 10 degrees C (4400 s-1). Experimentally recorded MEPCs were mathematically simulated to obtain a quantitative description of the processes controlling MEPC generation. Mathematical simulation further suggests that (i) acetylcholine diffusion kinetics may affect the onset rate of MEPCs without, however, being rate-limiting; and (ii) partial, transient acetylcholinesterase inhibition operated by acetylcholine may explain the low temperature sensitivity exhibited by the onset rate of MEPCs at high temperatures.

Modelling endplate currents: dependence on quantum secretion probability and decay of miniature current.

Quantification of the time course and amplitude of endplate currents (EPC) was made with respect to dispersion of quanta secretion and to changes in the exponential decay of miniature endplate currents (tau mepc). The relationship between RPC amplitude and tau mepc follows a double-exponential curve with tau1 = 0.3 ms and tau2 = 6 ms. If the amplitude of fully synchronised EPC is taken as 100%, then the loss of EPC amplitude is already 42% with "physiological" parameters of dispersion (the half-rise and decay constant of distribution of secretion probability = 0.5 ms, taumepc = 1 ms). This loss is even more substantial if secretion is more dispersed or miniature endplate currents decay faster.

The effect of non-quantal acetylcholine release on quantal miniature currents at mouse diaphragm.

1. The amplitude and exponential decay time constant of miniature endplate currents (MEPCs) were measured in mouse diaphragms treated with anti-cholinesterase under conditions known to modulate non-quantal acetylcholine (ACh) release. 2. Anti-cholinesterase prolonged MEPC decay and the extent of this initial prolongation was not influenced by non-quantal release. When non-quantal release was present, the decays of MEPCs became increasingly faster over several hours. This increased decay did not occur in the absence of non-quantal release. 3. Potentiation of the non-quantal release by zero Mg2+ and 1 x 10(-5) M choline, on the other hand, led to acceleration of MEPC shortening. 4. Increase of temperature from 15 to 26 degrees C and the presence of the desensitization-promoting drug proadifen (5 x 10(-6) M) accelerated the rate of MEPC shortening. 5. These observations are consistent with increased receptor desensitization due to non-quantal release. Repetitive binding of ACh to postsynaptic receptors which prolongs the time course of MEPC in anti-cholinesterase-treated endplates leads to progressive desensitization in the presence of non-quantal release and to the subsequent shortening of the quantal responses.

Effects of "non-quantal" acetylcholine on postsynaptic membrane senstitivity: Effects of ouabain, and mimicry by exogenous acetylcholine

The development of postsynaptic potentiation (PSP) and desensitization due to "non-quantal" acetylcholine that occurs when acetylcholinesterase (AChE) is inhibited was studied using the Na,K-ATPase inhibitor, ouabain, to alter (initially increasing, then decreasing) the level of non-quantal acetylcholine secretion, and exogenous acetylcholine. When ouabain increased non-quantal secretion the time constant (τ) of the miniature end-plate current (MEPC) decay increased, i.e., PSP developed. The later the application of ouabain relative to inhibition of AChE, the greater the degree of PSP. During the next phase when non-quantal secretion was inhibited the MEPC time course shortened more rapidly than in the controls, i.e., desensitization occurred. If ouabain abolished non-quantal secretion before AChE had been inhibited τ did not change, and neither PSP nor desensitization developed. When AChE was not inhibited ouabain had no effect on τ. When ACh was continuously applied at 20 nmol·liter−1, similar to the nonquantal concentration, the shortening of τ slowed down, and the signal amplitude declined more rapidly than in controls. Addition of exogenous ACh (50 nmol·liter−1) after acceleration of MEPC decay had developed caused τ to increase to its initial value. The combined appearance of PSP and desensitization during the action of non-quantal ACh, and the sustained desensitization after removal of released ACh from the synaptic cleft are discussed.

Effects of quantal content, membrane potential, and cholinoceptor density on the time course of end-plate currents in the rat under during acetylcholinesterase inhibition

The time-course of multiquantal end-plate currents (EPCs) was compared with monoquantal synaptic responses, i.e., miniature end-plate currents (MEPCs), in voltage-clamped rat diaphragm muscle fibers. In the presence of active acetylcholinesterase (AChE), the time constant of the decay of EPCs, that were composed of 25–140 quanta, was 1.2 times greater than that of MEPCs. After inhibition of AChE with armine or proserine the decay of the EPC was longer than the decay of the MEPC by 10–100 times, and unlike the MEPC, in the majority of synapses it could be described by the sum of two (n=34) or three (n=9) exponentials: monoexponential EPCs were noted in only three cases. The nature and duration of the EPC decay depended on its quantal content. After a reduction in the quantal content a three-exponential EPC decay could be successively reduced to a two- and a mono-exponential decay. A ,“slow,“ component of the EPC decay, unlike the MEPC decay, was extremely sensitive to changes in the membrane potential, and extracellular magnesium ion concentration. When the cholinoceptors were irreversibly blocked by α-bungarotoxin the MEPC decay accelerated, and the monoexponential EPC decay initially slowed down before accelerating, but even during a profound blockade the open-times of the ion channels were not affected. It therefore appears that during the generation of multiquantal EPCs when AChE is inhibited, not only does the synchronicity of the ion channel opening change, but so do their kinetics, possibly because of ion channel blockade by endogenous acetylcholine.

Inflammation at the neuromuscular junction in myasthenia gravis

To better define the pathogenic mechanisms in the antibody-mediated autoimmune disease myasthenia gravis (MG), we analyzed the morphology and electrophysiology of the neuromuscular junction in anconeus muscle biopsy specimens from eight patients with MG and seven control subjects. There were inflammatory cells at the neuromuscular junction in seven of the eight biopsies from MG patients. The endplate index (length of the postsynaptic membrane divided by the length of the apposed presynaptic membrane) was abnormally reduced in all the MG patients, and fiber type grouping, suggestive of reinnervation, was present in six of the eight MG patients. Intracellular recording revealed diminished amplitude of miniature endplate potentials and miniature endplate currents in the MG patients compared with the controls. The time constant of decay of miniature endplate currents did not differ from that of controls, suggesting no change in mean channel open time of the acetylcholine receptor. The endplate receptor sensitivity to iontophoretically applied acetylcholine was also decreased in MG patients compared with controls. The quantal content of neurally evoked endplate potentials was reduced in six of the eight MG patients, demonstrating abnormal presynaptic function as well. The presence of inflammatory cells at the neuromuscular junctions of limb muscles in MG reconciles an apparent disparity between the animal model of MG, experimental autoimmune myasthenia gravis, and the human disease. This study also demonstrates a frequent presynaptic component to the abnormal neuromuscular transmission in MG.

Effects of "non-quantal" acetylcholine on miniature endplate currents in mice

The possibility of postsynaptic potentiation (PSP) and desensitization developing due to nonquantal acetylcholine (ACh) secretion was investigated in mouse diaphragm with reference to time-amplitude relationships of miniature endplate currents (MEPC). The H effect (which characterizes nonquantal secretion (NS) of ACh) fell to zero over 3 h under the action of armine-induced inhibition of acetylcholinesterase (AChE) at a temperature of 20°C. A decline in the decay time constant (τ) of MEPC unaccompanied by observable alteration in MEPC amplitude occurred at the same time. This accelerated decay of MEPC was not observed in the absence of NS (the early stages of denervation). Start of NS did not show any effect on maximum retardation of MEPC decay due to AChE inhibition, indicating that no PSP sets in under the effects of non-quantal secretion. The effect of decline in τ accelerated with a rise in temperature; it could be reproduced with neostigmine replacing armine, while τ remained unchanged in the time spells investigated with AChE in its active state. Non-quantal ACh is not thought to produce substantial retardation of MEPC decay, although it does bring about desensitization, signs of which may be partially masked owing to concurrent onset of PSP.

The temperature dependence of the time course of growth and decay of miniature end-plate currents in carp extraocular muscle following thermal acclimation

1. The effect of temperature (5-35 degrees C) on the decay and growth phases of miniature end-plate currents (MEPCs) was investigated in extraocular muscle from freshwater carp acclimated to either high (28 degrees C) or low (8 degrees C) temperature. 2. The temperature dependence of the time constant of decay (TD) was found to follow an Arrhenius relationship; the relationship between logTD and reciprocal of absolute temperature (1/K) being linear in both groups. The TD of MEPCs recorded from cold-acclimated carp was not statistically significant from that of the warm group. 3. TD was moderately temperature-dependent. Regression gave a Q10 of 1.78 for the warm-acclimated carp, corresponding to an activation energy, Ea, of 41.15 +/- 2.17 kJ mol-1. For the cold-acclimated carp, the Q10 was 1.79, and Ea was 41.43 +/- 2.46 kJ mol-1. 4. Growth time (TG) was less susceptible than TD to temperature change. The relationship between growth time (taken as the time for MEPCs to rise from 20 to 80% of maximum) and temperature was linear for the cold-acclimated group, with a Q10 of 1.34 and Ea of 20.94 +/- 4.75 kJ mol-1. The data for the warm group, were, in contrast, best fitted by two linear regressions meeting at 15.1 degrees C. At temperatures below 15.1 degrees C Q10 was 3.16 and Ea was 82.20 +/- 15.47 kJ mol-1; above 15 degrees C, Q10 was 1.22 and Ea was 14.15 +/- 12.24 kJ mol-1. 5. The acetylcholinesterase inhibitor neostigmine increased TD by approximately twofold and raised TG to approximately 1.4 times control values. These effects were observed across the temperature range scanned for both groups. 6. The results are discussed with reference to the documented effects of temperature and temperature acclimation on membrane lipids and proteins.

Development of desensitization during repetitive end-plate activity and single end-plate currents in frog muscle.

1. The amplitudes of end-plate currents (EPCs) in short trains of fifteen to seventeen EPCs at 10 Hz were depressed in the presence of 10 microM-proadifen when acetylcholinesterase (AChE) was inhibited. 2. The proadifen-induced EPC depression was voltage-dependent and the effect was more pronounced at negative membrane potentials. 3. In the presence of proadifen, the mean amplitude of miniature end-plate currents (MEPCs) was reduced by 36% 5 s after the EPC train as compared with MEPCs before the train. 4. Without proadifen, but with inhibited AChE, an increase of temperature from 20 to 26 degrees C and elevation of external Ca2+ from 1.8 to 2.5 mM led to EPC amplitude depression in the train, which was also potential-dependent. 5. After AChE inhibition, proadifen (10 microM) progressively shortened MEPC decay without significant reduction of amplitude up to 40 min of exposition. MEPCs were not affected by proadifen when AChE was active. 6. It is concluded that these postsynaptic effects of proadifen can be explained neither by its action on the resting acetylcholine receptors (AChR) nor on open ion channels but are due to its desensitization-promoting action.

Changes in the properties of synaptic channels opened by acetylcholine in denervated frog muscle

Acetylcholine (ACh)-activated channels in end-plates of frog sartorius muscle were studied at various times after denervation. Mean open times of the synaptic membrane channels were derived from the time constant of decay of miniature end-plate currents ( τ MEPC) evoked by ACh quanta released from Schwann cells, which replace the motor nerve terminals after these degenerate. Membrane current noise, elicited by iontophoretic application of ACh to voltage-clamped end-plates, was also used to determine mean open time ( τ noise) and conductance of the ion channels. About 1 week after denervation, soon after Schwann cell MEPCs appeared. they had a τ similar to that of the neural MEPC in innervated end-plates. However, 5–6 weeks after denervation τ MEPC was increased by a factor of about 5. Circa 4 weeks after denervation, cholinesterase activity of the denervated muscle decreased to 76% of that in the contralateral, innervated muscle, and even 4 months after the operation it was still 64%. Thus, it is unlikely that a change in acetylcholinesterase activity is the main factor responsible for the increase in τ of Schwann cell MEPC. About 1 week after denervation τ noise was close to that in innervated end-plates (about 2 ms). Twelve to 24 days after denervation the average channel open time was 4.5 ± 1.0 ms, with some end-plates still showing normal ‘fast’ channels. However, in muscles denervated for 47–113 days the open time was 12.9 ± 1.9 ms. In the early and intermediate periods, ACh-induced noise spectra with two components were obtained from many end-plates, indicating the simultaneous activation of two different types of channels. At some end-plates during the early and intermediate periods after denervation, but not after about 5 weeks, neostigmine caused the appearance of a component, which was as fast as that of normal end-plate channels. In other experiments small doses of α-bungarotoxin were applied in order to predominantly block extra-junctional receptors. In the early period of denervation, when two components were present in the noise spectra, α-bungarotoxin eliminated the slow component leaving channels as fast as in innervated end-plates. After prolonged denervation, a component with τ of about 5.5 ms was occasionally disclosed by application of α-bungarotoxin. τ noise and τ MEPC from the same end-plate closely agreed. Our results indicate that at frog end-plates the open time of the majority of the synaptic channels opened by ACh becomes longer with increasing time after denervation.

A voltage clamp study of the glutamate responsive neuromuscular junction in Drosophila melanogaster.

The point and single electrode voltage clamp methods have been used to study the characteristics of junctional currents in Drosophila melanogaster larvae muscle fibers and the modulation of these currents by excitatory amino acids, short and long chain n-alkanols, and pentobarbital. The decay phase of junctional currents in Drosophila was found to be dominated by cooperativity in transmitter binding associated with reverberation, that is, repeated binding of transmitter with receptors as the transmitter molecules diffuse away from the active region. The current decay does not directly reflect the closure of ion channels and is qualitatively similar to the decay of miniature end-plate currents at the mouse neuromuscular junction after poisoning of acetylcholinesterase by paraoxon. In Drosophila an increase in membrane hyperpolarization both slows the time course of current decay and increases the degree of reverberation. The application of excitatory amino acids including glutamate, N-methyl-D-aspartate, quisqualate, and kainate causes a significant decrease in the amplitude of the junctional currents, a prolongation of the decay time course, and a reduction in reverberation of transmitter. The height of junctional currents is also diminished by the n-alkanols ethanol, pentanol, and octanol and by the barbiturate pentobarbital; ethanol also hastened the time course of decay of the currents.

Changes in miniature end-plate currents due to high potassium and calcium at the frog neuromuscular junction.

Elevation of extracellular potassium concentration ([K+]o) in cutaneous pectoris neuromuscular junction from 2 to 20 mM slowly increased the variability of the amplitudes of miniature end-plate currents (AMEPC-s), (coefficient of variation of AMEPC-s increased by 73%). Mean AMEPC-s, however, decreased but not markedly (by 14%). Comparable MEPC changes were observed when [K+] was raised in the presence of choline chloride (50 microM), arguing that MEPC changes were not primarily due to a lower and less uniform vesicular filling. Channel kinetics were not altered by high [K+]o, since the time constant of decay of miniature end-plate currents (TMEPC-s) did not change. Acetylcholine clearance from the synaptic cleft, however, appeared to be faster in high [K+]o since with cholinesterase blocked throughout, TMEPC-s were shortened. The changes of spontaneous quantal discharge induced by high [K+]o can be almost entirely explained by altered spatial distribution of vesicular release if, as recent reports suggest, at high [K+]o, exocytosis appears randomly not only at but also in between the active zones. However, relatively greater frequency of large MEPCs suggests that in high [K+]o some, and possibly all, quanta are filled above normal levels. High [Ca2+]o appears to counteract, although not always completely, all changes in spontaneous quantal secretion induced by high [K+]o. It is possible that high [Ca2+]o reverses the changes in the spatial distribution of vesicular release induced by high [K+]o. However, high [Ca2+]o also leads to other pre- and postsynaptic changes.

A further study on the kinetics of the subcellular current events at the mouse end-plate in the presence of cimetidine and ranitidine

The cholinomimetic activity of Cimetidine and Ranitidine has been demonstrated by several Authors. In the aim to better understand the phenomenon, we analyse the miniature end-plate current decay time. The prolongation of the decay phase of the synaptic current induced by the “selective” H2-antagonist Ranitidine, and to a lesser extent and at higher concentrations by Cimetidine, resembles that of the cholinesterase inhibitors. These agents usually prolong the quantal conductance change having little or no effect on the channel lifetime. The results of our previous experiments, which data were obtained by analyzing the “voltage” events, either spontaneous or evoked, of a classic frog preparation, showed a marked alteration of the temporal parameters. These effects, obtained at higher drug concentrations than those used in the present work, are now better defined by deriving extracellularly the “current” events. The results are also compared with those obtained by assaying the cholinesterase inhibitor Eserine, under the same experimental conditions.

Concentration-dependent effects of neostigmine on the endplate acetylcholine receptor channel complex

The concentration-dependent actions of neostigmine, a carbamate anticholinesterase agent, were studied on the acetylcholine receptor channel complex in voltage-clamped twitch fibers of costocutaneous muscles of garter snakes. Low concentrations of neostigmine (10(-6) or 10(-5) M) increased miniature endplate current (MEPC) amplitude and the time constant of MEPC decay without changing the relationship between the MEPC decay time constant and membrane potential. Acetylcholine- or carbachol-induced endplate current fluctuation spectra were well fitted by a single Lorentzian curve with a characteristic frequency and single-channel conductance unaltered by low concentrations of neostigmine. Concentrations of neostigmine greater than 5 X 10(-5) M decreased MEPC amplitude and split the decay of MEPCs into two components, one faster and one slower than the control rate. These effects were both voltage and concentration dependent. Spectra of current fluctuations recorded in concentrations greater than or equal to 5 X 10(-5) M neostigmine required two time constants, one faster and one slower than the control. Two component spectra were also obtained with carbachol-induced current fluctuation spectra, indicating that these effects of neostigmine were direct and not a consequence of acetylcholinesterase inhibition. Similar results were also obtained in muscles pretreated with collagenase to remove junctional acetylcholinesterase. The fast and slow time constants obtained from current fluctuation spectra decreased and increased, respectively, with either increases in the concentration of neostigmine or membrane hyperpolarization when analyzed in the same fiber. The effects of neostigmine on channel lifetime were reversible with washing. These results indicate that the effects of neostigmine are concentration dependent. Concentrations greater than 2.5 X 10(-5) M exhibit direct effects on the endplate receptor channel complex which are unrelated to acetylcholinesterase inhibition. These actions include: a prolongation of the gating kinetics of the endplate receptor channel complex, the production of an altered state of the receptor channel complex evidenced by a high frequency component to current fluctuation spectra, and a direct action to block the acetylcholine receptor.

Postsynaptic block of frog neuromuscular transmission by conotoxin GI

Conotoxin GI, a peptide neurotoxin contained in the venom of the marine snail Conus geographus, was applied to the cutaneous pectoris muscle of the frog, and the effects on the postsynaptic response to acetylcholine were examined. Conotoxin GI reversibly blocked nerve-evoked muscle contractions at concentrations greater than or equal to 3 to 4 microM. Micromolar concentrations of conotoxin GI significantly reduced the amplitude of miniature endplate potentials and membrane depolarizations produced by ionophoretic application of acetylcholine, suggesting that the toxin reduced the postsynaptic sensitivity to acetylcholine. The reduction in the sensitivity of the muscle to acetylcholine was not due to changes in muscle fiber resting membrane potential or input resistance. Conotoxin GI reduced the amplitudes but did not affect the rates of decay of focal, extracellularly recorded endplate currents or miniature endplate currents, suggesting that the toxin did not affect the lifetime of ion channels opened by acetylcholine. Miniature endplate currents decay five to six times more slowly than normal when acetylcholinesterase is blocked with neostigmine methyl sulfate due to repeated binding of acetylcholine to receptors as it diffuses from the synaptic cleft. Conotoxin GI reduced the amplitude and increased the rate of decay of miniature endplate currents recorded in the presence of neostigmine methyl sulfate, suggesting that the toxin reduced the binding of acetylcholine to endplate receptors. These results are consistent with the hypothesis that conotoxin GI blocks neuromuscular transmission at the frog endplate by reducing the binding of acetylcholine to receptors.

Factors determining the duration of a single postsynaptic response in neuromuscular junctions

The miniature end-plate currents (MEPCs) and acetylcholine-induced current fluctuations were compared in experiments on fast and slow muscle fibres of lamprey, frog, chicken and rat. Simultaneous analysis of MEPCs decay time constant and mean life-time of single ionic channels suggests that the former is the main but not the sole factor determining the MEPCs duration. Additional factors, in particular, the relative insufficiency of acetylcholinesterase activity (AChE) are more important for the generation of the usual MEPSs in slow muscle fibres or the "giant" MEPCs in fast ones. Low activity of AChE favours the prominent asynchrony of interaction between acetylcholine molecules and cholinoreceptors causing prolongation of the time course of synaptic response. The mechanisms of MEPCs decay shortening induced by alpha-bungarotoxin or d-tubocurarine and the nonuniformity of different active spots of junctions are discussed.

Miniature end plate currents from teleost extraocular muscle

Miniature end plate currents (MEPCs) were recorded with focal extracellular electrodes from white extraocular muscle fibres of a marine teleost fish,Trachurus novaezelandiae, over a temperature range of 5 °C to 27 °C. 1. Teleost MEPCs rose rapidly, attaining a maximum amplitude of 250–500 μV, withTGof about 150 μs at 15 °C (Figs. 1, 2). 2. Decay of MEPCs was exponential, with τ=1 ms at 15 °C (Figs. 3, 5). τ was an exponential function of absolute temperature, withEa=70 kJ (Fig. 5). 3. τ ofTrachurus MEPCs was consistently smaller than values of τ reported for other vertebrate end plates (Table 1). Low τ is correlated with a high degree of lipid unsaturation in teleosts, and may be caused by increased membrane fluidity. 4. Frequency distributions ofTG(Fig. 2) and τ (Fig. 4) at a single recording site appear to represent one population of events, skewed toward smaller values. 5. Teleost MEPCs also appeared to be normal cholinergic MEPCs in that their rates of decay were decreased by neostigmine, ethanol and membrane hyperpolarization.