Characteristics of postsynaptic potentials and ionic currents in synapses of fast and slow rat muscle fibers

Miniature end-plate currents and potentials (MEPPs and MEPCs, respectively) were recorded in fast and slow rat muscle fibers by extracellular focal recording and voltage clamp techniques. The rise time and the half-decay time of these potentials and currents were 1.3–1.4 times greater in slow fibers than in fast. A similar difference, but lesser in degree, also was observed after inhibition of acetylcholinesterase. Decline of the end-plate currents remained, generally speaking, exponential and its rate depended on the clamped voltage. The percentage distribution of fibers of different types by duration of MEPP and MEPC in fast and slow muscles correlated with the percentage distribution of fibers identified in these muscles on the basis of other parameters. Factors determining the time course of the responses (acetylcholinesterase activity, length of diffusion pathways, differences in passive electrical properties of the membrane), and their importance for synapses of different types, are discussed.I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya, Vol. 12, No. 6, pp. 627–636, November–December, 1980.     

Postsynaptic currents in phasic and tonic muscle fibers of the rat extraocular muscle

Focal extracellular recordings were made of postjunctional currents produced at synapses of the inferior rectus eye muscle fibers by the spontaneous release of quanta of transmitter. These consisted of miniature endplate currents, or MEPC, in phasic fibers and miniature postjunctional currents, or MPJC, in tonic fibers. Open time of ionic channels (_chan) was also registered. In tonic fibers, MPJC lasted considerably longer than MEPC did in phasic fibers: rising time, decay time, and _chan in the former measured respectively 2.5, 4–5, and 2.2 times higher than in the latter. Acetylcholinesterace (AChE) inhibition produced a much greater (4.4-fold extension of current decay in phasic than in tonic fibers, where a 1.8-fold increase was seen, thereby reducing the gap between the decay time of currents in these fibers to a difference of 1.6 times. The more protracted decay of MPJC in tonic fibers compared with MEPC in phasic fibers is determined by the lower functional activity of AChE as well as the higher value of _chan. Duration of MEPC and magnitude of _chan in the "slow" phasic fibers of rat skeletal muscles fell well below the same parameters measured in the tonic fibers of the ocular muscle.I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya, Vol. 19, No. 1, pp. 120–129, January–February, 1987.     

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 -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.S. V. Kurashov Institute of Medicine, Russian Ministry of Public Health, Kazan. Translated from Neirofiziologiya, Vol. 24, No. 3, pp. 269–279, May–June, 1992.     

Miniature endplate currents of muscle fibers from rat diaphragm during galantamine-induced acetylcholinesterase inhibition

Miniature endplate currents (MEPC) were recorded in muscle fibers of rat diaphragm using voltage clamp technique during acetylcholinesterase (AChE) inhibition induced by various concentrations of galantamine. Their amplitude and time course began to increase at a galantamine concentration of 3.16·10^–8 g/ml. Increased concentrations of galantamine produced a greater effect. Maximum amplitude and time course were reached at a concentration of 10^–6 g/ml. The input resistance of muscle fibers increased under the effects of galantamine. In all cases MEPC fell exponentially. At a concentration of 10^–5 g/ml galantamine produced a curarelike effect; amplitude and time course of decay increased to a lesser extent than at a concentration of 10^–6 and the decay in MEPC became biphasic. Following washout of galantamine (10^–5 g/ml) the time course of MEPC first rose, then fell, returning to the initial level in 3 h, and decay again became exponential. Changes in MEPC parameters under the effects of different concentrations of galantamine and washout were closely correlated. A positive correlation was found between the time course of decay and MEPC amplitude both in the presence and absence of AChE inhibition. It is postulated that the functional importance of synaptic AChE in repressing the postsynaptic action of acetylcholine is limited and that parameters of postsynaptic response may therefore be used to evaluate its action.A. A. Ukhtomskii Institute of Physiology, A. A. Zhdanov State University, Leningrad. Translated from Neirofiziologiya, Vol. 17, No. 5, pp. 607–614, September–October, 1985.     

Modelling of miniature endplate current

From analyzing the mathematical model of miniature endplate current (MEPC) generation described previously an optimal set of parameters was found providing the best match between the results of stimulation and experimentally obtained findings. The time course of MEPC in the controls, after cholinesterase inhibition, and following a bungarotoxin-induced reduction in the density of unoccupied cholinoreceptors were described within the framework of the model. This model also statisfactorily describes voltage-dependent current decay, and the currentvoltage relationship of MEPC, as well as the kinetics of giant MEPC observed during cholinesterase inhibition. The influence of the parameters of the model on model MEPC is also examined. The good match between the results of modelling and experimental findings leads to the conclusion that the model gives a true picture of different processes contributing to the generation of MEPC.S. V. Kurashov Medical Institute, Kazan', Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya Vol. 20, No. 3, pp. 390–397, May–June, 1988.     

Postsynaptic potentiation and desensitization at the frog neuromuscular junction produced by repeated stimulation of the motor nerve

Investigations were performed on a split neuromuscular preparation of frog sartorial muscle during acetylcholinesterase inhibition. A study was made of the part played in postsynaptic potentiation (PSP) and desensitization (DS) in changes in the amplitude and time course of miniature endplate currents (MEPC) recorded directly after regular stimulation of the motor nerve at a frequency of 10 Hz for 5 or 60 sec, producing short and long series of multiquantal endplate currents (EPC) respectively. After the short train the amplitude of MEPC could hardly be distinguished from initial level, while the decay time constant (MEPC) increased by 32%, indicating PSP. Comparable but more pronounced biphasic changes occurred in the time course of endplate currents. These effects were not observed when acetylcholinesterase was uninhibited. Both PSP and DS were restored when 1×10^–6 M exogenous acetylcholine was added to the bath. The ratio between them could be changed by aprodifen — a substance which accelerates desensitization.S. V. Kurashov Medical Institute, Ministry of Public Health of the RSFSR, Kazan'. I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya, Vol. 18, No. 5, pp. 645–654, September–October, 1986.     

Reactivating and cholinolytic action of trimedoxime bromide at the neuromuscular junction of warm-blooded animals

The reactivating and cholinolytic action of trimedoxime bromide was evaluated during experiments on rat soleus and diaphragm muscles accoridng to the amplitude and time course of miniature end-plate potentials and currents (MEPP and MEPC respectively). This agent reactivates acetylcholinesterase (AChE) phosphorylation. The effects of trimedoxime bromide at concentrations of 5·10^–6–5·10^–4 M following AChE inhibition on the amplitude and duration of MEPP arises from complex interaction between the reactivating and cholinolytic effects. A separate evaluation of the reactivating effect (once the reactivating agent had been removed) revealed that this action increases throughout the entire range of trimedoxime bromide concentration: complete reactivation of AChE phosphorylation was observed under the action of 2–5·10^–4 M trimedoxime bromide. Examination of the cholinolytic effect in isolation (with voltage-clamping at the muscle and intact AChE) showed that blockade of open end-plate ionic channels underlies this effect. Reduction in MEPC amplitude together with retarded (but still exponential) decay of signals were distinguishing features of this blockade, confirming that trimedoxime bromide acts as a very fast blocker.S. V. Kurashov Medical Institute, Ministry of Public Health of the RSFSR, Kazan'. Translated from Neirofiziologiya, Vol. 20, No. 3, pp. 351–357, May–June, 1988.     

Slow asymmetric currents and tubulo-reticular junction ultrastructure in crayfish muscle fibers

Asymmetric membrane currents in isolated muscle fibers of the crayfishAstacus fluviatilis were studied under voltage clamp conditions with controlled composition of the external and internal medium. Besides fast asymmetric currents which are probably associated with opening of calcium channels in the surface membrane, slow asymmetric currents with a time course almost an order of magnitude slower than in fast frog muscle fibers also are present in fibers of this type. The value of the charge transported across a single "foot" in the tubulo-reticular junction was calculated. The number of feet and their arrangement in each junction were studied by transmission electron microscopy. The number of charges transported across one foot agrees with the hypothesis that slow displacement currents are linked with movement of charge particles distributed over the whole area of the sarcolemmal and tubular invaginations, and not only in the feet.Center for Physiological Sciences, Slovak Academy of Sciences, Bratislava, Czechoslovakia. Translated from Neirofiziologiya, Vol. 16, No. 5, pp. 612–619, September–October, 1984.     

Muscle remodeling in adult snapping shrimps via fast-fiber degeneration and slow-fiber genesis and transformation

Bilateral asymmetry of the paired snapper/pincer claws may be reversed in adult snapping shrimps (Alpheus heterochelis). Removal of the snapper claw triggers transformation of the contralateral pincer claw into a snapper and the regeneration of a new pincer claw at the old snapper site. During this process the pincer closer muscle is remodeled to a snapper-type, and these alterations have been examined with the electron microscope. There is selective death of the central band of fast fibers, accompanied by an accumulation of electron-dense crysttaline bodies in the degenerating fibers. Two principal types of hemocytes (amebocytes and coagulocytes) invade the area and the degenerating muscle fibers. New myotubes also appear in this central site. The myotubes are characterized by a prolific network of presumptive sarcoplasmic reticulum and transverse tubules, nascent myofibrils, and crystalline bodies. The myotubes are innervated by many motor nerve terminals, and they subsequently differentiate into long-sarcomere (8–12 m), slow muscle fibers. Remodeling of the central band, therefore, occurs by degeneration of the fast fibers and their replacement by new slow fibers. Remnants of the degenerating fast fibers act as scaffolding for the myotubes which originate from adjacent satellite cells. The crystalline bodies may represent protein stores from the degeneration of the fast fibers, recycled for use in the genesis of new fibers. The invading hemocytes appear to play several roles, initially phagocytosing the fast muscle fibers, transporting the crystalline bodies into the new myotubes, and acting as stem cells for the new muscle fibers. Apart from the central band of fibers, the remaining pincer-type slow fibers with sarcomere lengths of 5–7 m are transformed via sarcomere lengthening into snapper-type slow fibers with sarcomere lengths of 7–12 m. Thus, during claw transformation in adult snapping shrimps, the pincer closer muscle is remodeled into a snapper closer muscle by selective death of the fast-fiber band, replacement of the fast-fiber band by new slow fibers, and transformation of the existing slow fibers to an even-slower variety. Note. This paper is dedicated to the fond memory of Professor M.S. Laverack whose enjoyment of biological research and gentle encouragement of such endeavours touched all those who knew him.     

Postsynaptic end-plate ionic currents in fast and slow chick muscle fibers. Effect of cholinesterase inhibition

Miniature end-plate potentials (MEPPs) were recorded in fast and slow chick muscle fibers extracellularly (focally) and under voltage clamp conditions. The duration of the MEPPs in synapses of slow fibers was on average 2.5 times longer than their duration in synapses of fast fibers. Inhibition of acetylcholinesterase (AChE) lengthened MEPPs by a varied degree: by 1.5 times in synapses of slow fibers and by 3.5 times in those of fast fibers. As a result the difference in the decay time of MEPPs in synapses of these types disappeared almost completely, and only a small difference remained in the rise time of the MEPPs. The MEPP decay time during hyperpolarization in the slow fiber synapse was rather less dependent on potential than in synapses of fast fibers; after inhibition of AChE it became even less dependent. Similar changes in potential dependence were found after lengthening of the MEPP by the action of ethanol. The functional significance of differences in AChE activity and in the activating effect of the mediator for the kinetics of MEPPs in synapses of fast and slow fibers is discussed.I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya, Vol. 13, No. 4, pp. 390–397, July–August, 1981.     

Two open states or two different Na channels in skeletal muscle fibers: Markov models of the decay of Na currents in frog skeletal muscle

The rate of sodium current decay at –140 mV was studied as a function of the duration and amplitude of the activating voltage pulse. These sodium current decays or tails of current showed a biexponential decline in amplitude which depended upon the duration of the activating pulse. At 12°C, the two exponential components of the Na tail currents exhibited time constants of 72 and 534 s. As the duration of an activating pulse was lengthened, the relative amplitude of the slow component of the decay increased compared to the fast component, without any changes in the fast and slow time constants. This slowing of the decay of current as a function of the duration of the activating pulse is found only in fibers with inactivation intact.A number of Markov models were tested for their ability to predict the biexponential decays found in muscle fibers with inactivation intact and removed. A homogeneous population of channels having only a single open state fails to predict the behavior. A homogeneous population of channels having two open states predicts the behavior. The behavior can also be predicted by two different types of single open-state sodium channels, with one ensemble of channels carrying a minority of the current and exhibiting a much slower closing rate. If a homogeneous population of channels is present, the simulations show that the observed changes in decay rates are driven by inactivation.     

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 () 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 accelerated with a rise in temperature; it could be reproduced with neostigmine replacing armine, while 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.S. V. Kurashov Medical Institute, Kazan'. Translated from Neirofiziologiya, Vol. 22, No. 4, pp. 507–513, July–August, 1990.     

Polarized distribution of γ interferon-stimulated MHC antigens and transferrin receptors in a clonal cell line isolated from Fisher rat thyroid (FRT cells)

Summary The fine structure of single identified muscle fibers and their nerve terminals in the limb closer muscle of the shore crab Eriphia spinifrons was examined, using a previous classification based on histochemical evidence which recognizes a slow (Type-I) fiber and three fast (Type-II, Type-III, Type-IV) fibers. All four fiber types have a fine structure characteristic of crustacean slow muscle, with 10–12 thin filaments surrounding each thick filament and sarcomere lengths of 6–13 m. Type-IV fibers have sarcomere lengths of 6 m while the other three types have substantially longer sarcomeres (10–13 m). Structural features of nerve terminals revealed excitatory innervation in all four fiber types but inhibitory innervation in Type-I, Type-II, and Type-III fibers only. Thus fibers with longer sarcomeres receive the inhibitor axon but those with shorter sarcomeres do not. Amongst the former, synaptic contact from an inhibitory nerve terminal onto an excitatory one, denoting presynaptic inhibition, was seen in Type-I and Type-II fibers but not in Type-III and Type-IV fibers. Inhibitory innervation of the walking leg closer muscle is therefore highly differentiated: some fibers lack inhibitory nerve terminals, some possess postsynaptic inhibition, and some possess both postsynaptic and presynaptic inhibition.     

Effects of hyaluronidase on miniature endplate potentials and currents at the frog neuromuscular junction

The effects of 0.1% testicular hyaluronidase on miniature endplate potentials and currents (MEPP and MEPC) were investigated in frog pectorocutaneous muscle. The action of hyaluronidase on preparations with armine-induced blockade of acetylcholinesterase was associated with decreased amplitude and duration of MEPP and MEPC half-decay time and rising phase. The correlation between amplitude and half-decay time of MEPP and MEPC declined at the same time, while MEPC decay remained exponential. Treating preparations having intact acetylcholinesterase with hyaluronidase increased the length of MEPC halfdecay, with duration of the rising phase and amplitude remaining constant. It is suggested that enzymatic breakdown of a proportion of the glycocalix of cells forming the neuromuscular junction and a portion of the extracellular matrix at the synaptic cleft leads to attenuation of nonspectific acetylcholine binding, thus facilitating acetylcholine diffusion into the synaptic cleft.A. A. Zhdanov State University, Leningrad. Translated from Neirofiziologiya, Vol. 20, No. 1, pp. 113–119, January–February, 1988.     

Postsynaptic potentiation of miniature endplate currents in rat diaphragm muscles. Effects of acetylcholinesterase inhibition,temperature, and curare

Miniature endplate potentials (MEPC) were recorded from rat diaphragm muscle fiber. A positive correlation was found in controls between half-decay time and amplitude of individual MEPC, an effect enhanced by acetylcholinesterase (AChE) inhibition (correlation coefficients: 0.29 and 0.49 respectively at a temperature of 28°C). Adding curare following AChE inhibition produced a reduction in the amplitude and duration of MEPC without influencing the correlation relationship between the above-mentioned parameters. This relationship declined significantly with a temperature reduction to 18°C in both the control and cases of AChE inhibition. The increase in MEPC half-decay time following AChE inhibition was greater at 28° than at 18°C; Q₁₀ equalled about two for duration of rising time as compared with around three for MEPC half-decay time. Factors determining the time course of MEPC are discussed. The findings obtained are explained by postsynaptic potential (and cooperative binding of agonists to cholinoreceptors lies at the root of this) and by the pattern of ACh diffusion at the synaptic cleft.A. A. Ukhtomskii Institute of Physiology, A. A. Zhdanov State University, Leningrad. Translated from Neirofiziologiya, Vol. 19, No. 4, pp. 504–512, July–August, 1987.     

Molecular Mechanisms of Regulation of the Activity of Sarcoplasmic Reticulum Ca-Release Channels (Ryanodine Receptors), Muscle Fatigue, and Severin''s Phenomenon

In this short review of the literature and our own data the characteristics of structural organization of sarcoplasmic reticulum Ca-release channels (ryanodine receptors) in different types of muscles, the participation of other sarcoplasmic reticulum proteins in excitation–contraction coupling and Ca-release channel operation, and the regulation of the channel activity by endogenous low molecular weight compounds are analyzed. Special attention is given to changes that occur in muscle cells during exhausting work and to the role of sarcoplasmic reticulum Ca-release channels in the loss of muscle contractile activity during the development of fatigue. It is concluded that the protection of muscle fibers against fatigue in the presence of the histidine-containing dipeptide carnosine, called in the literature Severin's phenomenon, is primarily connected with modulation of sarcoplasmic reticulum Ca-release channel activity by carnosine.     

The single-channel basis for the slow kinetics of synaptic currents in vertebrate slow muscle fibers

The time course of synaptic currents is significantly longer in slow than in fast twitch muscle fibers. To examine the underlying basis for these slow synaptic currents, single-channel recordings were made from the synapses of slow muscle fibers. Our analysis indicates that low conductance acetylcholine receptor (AChR) channels predominate in innervated slow fibers. The high level of expression of low conductance channels is in contrast to fast twitch fibers, in which these channels are expressed in significant numbers only in embryonic or denervated muscle. Analysis of the distribution of open durations for the low conductance channel class suggests that the open time of this AChR class is the major determinant in shaping the slow time course of synaptic current decay. The predominant contribution of low conductance channel openings to synaptic currents of slow muscle fibers indicates a well-defined physiological role for this class of AChRs.     

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 () 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 did not change, and neither PSP nor desensitization developed. When AChE was not inhibited ouabain had no effect on . When ACh was continuously applied at 20 nmol·liter^–1, similar to the nonquantal concentration, the shortening of 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 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.S. V. Kurashova Institute of Medicine, Russian Federation Ministry of Public Health, Kzan. Translated from Neirofiziologiya, Vol. 24, No. 4, pp. 396–404, July–August, 1992.     

Development of chicken intrafusal muscle fibers

The first sign of developing intrafusal fibers in chicken leg muscles appeared on embryonic day (E) 13 when sensory axons contacted undifferentiated myotubes. In sections incubated with monoclonal antibodies against myosin heavy chains (MHC) diverse immunostaining was observed within the developing intrafusal fiber bundle. Large primary intrafusal myotubes immunostained moderately to strongly for embryonic and neonatal MHC, but they were unreactive or reacted only weakly with antibodies against slow MHC. Smaller, secondary intrafusal myotubes reacted only weakly to moderately for embryonic and neonatal MHC, but 1–2 days after their formation they reacted strongly for slow and slow-tonic MHC. In contrast to mammals, slow-tonic MHC was also observed in extrafusal fibers. Intrafusal fibers derived from primary myotubes acquired fast MHC and retained at least a moderate level of embryonic MHC. On the other hand, intrafusal fibers developing from secondary myotubes lost the embryonic and neonatal isoforms prior to hatching and became slow. Based on relative amounts of embryonic, neonatal and slow MHC future fast and slow intrafusal fibers could be first identified at E14. At the polar regions of intrafusal fibers positions of nerve endings and acetylcholinesterase activity were seen to match as early as E16. Approximately equal numbers of slow and fast intrafusal fibers formed prenatally; however, in postnatal muscle spindles fast fibers were usually in the majority, suggesting that some fibers transformed from slow to fast.     

Effects of voltage and temperature changes on postsynaptic potentiation at the frog neuromuscular junction

The difference in the decay time constants of multiquantal endplate currents (EPC) produced by presenting paired stimuli 100 msec apart was measured during experiments on transversely cut neuromuscular preparations of the frog sartorius muscle. When acetylcholinesterase was inhibited by 3×10^–6 M prostigmine, decay time of the 2nd EPC (₂) was 39±8% longer than that of the first (₁) due to postsynaptic potentiation. It was found that degree of potentiation was not affected by membrane potential level within the –30 to –120 mV range. Several effects were produced by a drop in temperature: an increase in EPC decay time constant and in that of miniature endplate currents (MEPC) in particular, a slight drop in MEPC amplitude, and a reduction in EPC quantal content. By comparing paired EPC of equal quantal content at different temperatures it was found that potentiation was more pronounced at 12°C than at 22°C and the temperature coefficient Q₁₀ at which ₂ exceeds ₁ was 2.0±0.2 (n=7). The processes determining postsynaptic potential are clearly not voltage-dependent but have a complex dependence on temperature. Quantal content of EPC falls with reduced temperature, thereby restraining potentiation, while helping to retain residual transmitter activity.I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Kurashov Medical Institute, Kazan'. Translated from Neirofiziologiya, Vol. 18, No. 4, pp. 512–518, July–August, 1986.