Synaptic potential in the motor giant axon of the crayfish

Some electrical properties of the synapses between central giant axons (presynaptic) and the motor giant axon (postsynaptic) of the crayfish abdominal nerve cord have been investigated. Postsynaptic potential change in response to presynaptic volleys contains two components: a spike potential and a synaptic potential of very long time course. Amplitude of the synaptic potential is graded according to the number of active presynaptic axons. Conductance increase in the synaptic membrane endures over most of the period of potential change, and it is this rather than the "electrical time constant" of the membrane that in large measure determines the form of the synaptic potential. Temporal summation of synaptic potential occurs during repetitive presynaptic stimulation, and after such stimulation the rate of decay of synaptic potential is greatly slowed.     

Effects of 4-aminopyridine on the action potential and the after-hyperpolarization of cat spinal motoneurons

In cats under pentobarbital anaesthesia, intramotoneuronal administrations of 4-aminopyridine significantly prolong the falling phase of the antidromic action potential but have much less effect on the orthodromic action potential. 4-aminopyridine probably blocks the fast K channels involved in the repolarization of the membrane and indirectly activates ionic channels through enhancement of synaptic transmission, also suggested by the potentiation of excitatory postsynaptic potentials. In many cells, 4-aminopyridine depresses the amplitude and prolongs the time course of the after-hyperpolarization; therefore 4-aminopyridine may also partly block Ca2+-activated K+ channels.     

Effects of temperan a central synapse between identified motor neurons in the locust

Summary Changing the temperature from 10–40 °C modifies the transmission at an established monosynaptic connection between the fast extensor tibiae (FETi) and flexor tibiae motor neurons in the metathoracic ganglion of the locustSchistocerca gregaria (Forskål). Striking changes occur to the shape of the spikes, to membrane resistance, to the synaptic delay, and to the evoked synaptic potentials.In the presynaptic FETi motor neuron, raising the temperature reduces the amplitude of an antidromic spike recorded in the soma by a factor of 10 (40 mV to 4 mV), reduces the time taken to reach peak amplitude by 5 (3.5 to 0.7 ms) and decreases the duration at half maximum amplitude by 0.5. The conduction velocity of the spike in the axon is increased by 50% from 10 °C to 40 °C. Orthodromic spikes are affected by temperature in a similar way to the antidromic spikes.The membrane resistance of both pre- and postsynaptic motor neurons falls as the temperature is raised. The membrane resistance of FETi falls by a factor of 4 (about 4 M at 10 °C to 1 M at 40 °C). A contributory component to this fall could be the increase in the frequency of synaptic potentials generated as a result of inputs from other neurons. No temperature dependence could be demonstrated on the voltage threshold relative to resting potential for evoking orthodromic spikes, but because the resistance changes, the current needed to achieve this voltage must be increased at higher temperatures.The latency measured from the peak of the spike in the soma of FETi to the start of the EPSP in the soma of a flexor motor neuron decreases by a factor of 20 (10 ms at 10 °C to 0.5 ms at 40 °C).In a postsynaptic flexor tibiae motor neuron, the amplitude of the evoked synaptic potential increases by a factor of 3.4 (5 mV to 17 mV), its duration at half maximum amplitude decreases by 3 (7 ms at 12 °C to 2.3 ms at 32 °C) and its rate of rise increases by 3. An increased likelihood that spikes will occur in the flexor contributes to the enhanced amplitude of the compound EPSP at temperatures above 20 °C.Abbreviation FETi fast extensor tibiae motor neuron     

Presynaptic augmentation induced by NaF in sympathetic ganglion of bullfrog

Effects of NaF on the synaptic transmission of bullfrog sympathetic ganglia were studied by extra- and intracellular recordings. The results obtained were as follows: 1) The amplitude of the orthodromic compound action potential (CAP) evoked by preganglionic nerve stimulation was remarkably augmented with 10 microM NaF, whereas that of the antidromic CAPs remained unchanged with the same dose of NaF. The low amplitude of the orthodromic CAP which was diminished by a low-Ca2(+)-ringer's solution reversed with an additional administration of NaF. The amplitudes of the orthodromic CAPs were enhanced by phosphodiesterase inhibitors such as isobutylmethylxanthine, theophylline, and physostigmine. In addition, augmentation of the orthodromic CAPs was induced by an adenylate cyclase activator (forskolin) and d.b-cAMP; however, its augmented responses were not affected by an additional administration of NaF. 2) In the intracellular recording, NaF showed no effect on the resting membrane potential and depolarizing response induced by acetylcholine. However, the EPSP appearing in the phase of afterhyperpolarization of the orthodromic action potential was significantly increased by NaF, whereas no effect was found on the antidromic action potential. In order to evaluate these findings, effects of NaF on the decreased low-Ca2(+)-action potential were observed. After application of NaF, the low-Ca2(+)-orthodromic EPSPs were reversed, and when the height of the EPSP was raised to the critical firing level, a spike potential was driven in the cell. These facts suggest that the site of NaF action seems to exist in the presynaptic rather than postsynaptic process. Furthermore, it suggests that NaF probably acts on Gs-protein which activates adenylate cyclase at the presynaptic membrane. This resulted in a great increase in intracellular cAMP at the synaptic terminal and it triggered the Ca2(+)-increase. As an inevitable consequence, release of transmitter from the nerve terminals of the frog sympathetic ganglion was finally facilitated. These factors supposedly resulted in augmentation of the amplitude of the orthodromic CAP.     

Electrical properties of the dendrite in an insect mechanoreceptor: Effects of antidromic or direct electrical stimulation

A study of the negative phase of the spikes recorded extra cellularly from insect mechanoreceptor has been performed in order to characterize some electrical properties of the dendrite which contains the transducing part of the sensory neuron. These properties have been investigated in mechanoreceptors of the metathoracic leg of the locust Schistocerca gregaria by firing antidromic action potentials both at rest and during mechanical or electrical stimulation. The amplitude of the negative phase of the spike appears to be correlated with the polarization of the dendritic membrane, although when bursts of action potentials are applied, the relation is more complex, including a depressive influence of a given spike on the following spike. The receptor potential and the antidromic dendritic spikes both originate in the same region of the dendrite but they involve different ionic processes. Our results indicate that the dendrite is electrically excitable. The spike which originates in the dendrite has an initial negative phase with a small superimposed positive component. A spike of this shape is never observed under natural stimulation. It is proposed that the negative phase of the antidromic impulse provides a suitable means for studying the variations in electrical polarization of the dendrite which cannot be recorded directly.     

Effect of guanidine on the squid giant synapse

Effects of guanidine on pre- and postsynaptic activities in the untreated or tetrodotoxin-treated squid giant synapses were examined by externally perfusing with various concentrations (423 mM, 42 mM, 21 mM, and 4.2 mM), or by iontophoretic injection of guanidine into the presynaptic terminal. In 423 mM guanidine (Na-free), the pre- and postsynaptic spikes together with PSP were completely abolished. In concentrations of 42 mM or lower of guanidine media the following changes related to the concentration used were observed: reduction of delayed rectification of both axon membranes without significant alteration of resting membrane resistances; a few millivolts decrease in the resting membrane potentials; small decrease in amplitude of pre- and post-synaptic spikes without marked increase of spike duration; enhancement of synaptic activity as manifested by increases in the amplitude and duration of the PSP. Iontophoretically injected guanidine also reduced delayed rectification of the presynaptic membrane. Input-output relation was modified in a way similar to externally applied guanidine and an “Off-PSP” was demonstrated shortly after application of an inside positive presynaptic polarization. Thus, a comparison of the augmentation of synaptic transmission by the extracellular and intracellularly applied guanidine demonstrates that the primary effect is at the presynaptic terminal.     

Impact of fast sodium channel inactivation on spike threshold dynamics and synaptic integration

Neurons spike when their membrane potential exceeds a threshold value. In central neurons, the spike threshold is not constant but depends on the stimulation. Thus, input-output properties of neurons depend both on the effect of presynaptic spikes on the membrane potential and on the dynamics of the spike threshold. Among the possible mechanisms that may modulate the threshold, one strong candidate is Na channel inactivation, because it specifically impacts spike initiation without affecting the membrane potential. We collected voltage-clamp data from the literature and we found, based on a theoretical criterion, that the properties of Na inactivation could indeed cause substantial threshold variability by itself. By analyzing simple neuron models with fast Na inactivation (one channel subtype), we found that the spike threshold is correlated with the mean membrane potential and negatively correlated with the preceding depolarization slope, consistent with experiments. We then analyzed the impact of threshold dynamics on synaptic integration. The difference between the postsynaptic potential (PSP) and the dynamic threshold in response to a presynaptic spike defines an effective PSP. When the neuron is sufficiently depolarized, this effective PSP is briefer than the PSP. This mechanism regulates the temporal window of synaptic integration in an adaptive way. Finally, we discuss the role of other potential mechanisms. Distal spike initiation, channel noise and Na activation dynamics cannot account for the observed negative slope-threshold relationship, while adaptive conductances (e.g. K+) and Na inactivation can. We conclude that Na inactivation is a metabolically efficient mechanism to control the temporal resolution of synaptic integration.     

Synaptic transmission in the sixth ganglion of the cockroach: action of 4-aminopyridine.

1. Study was made of the action of 4-aminopyridine (5 X 10(-5) M) on synaptic transmission in the last abdominal ganglion of Periplaneta americana. The 'oil-gap' technique was used to record postsynaptic events in a single giant axon. 2. 4-AP quickly increased the 'background' of postsynaptic activity, which consisted of 'spontaneous' unitary EPSPs and IPSPs. Postsynaptic spikes were also propagated. 3. Both evoked EPSPs (stimulation of cercal nerve XI) and evoked IPSPs (stimulation of cercal nerve X) were greatly increased in amplitude although their duration (half-time) was unaltered. 4. 4-AP triggered presynaptic action potentials in the cercal nerves (recorded with external electrodes). These 'antidromic' potentials appeared singly or sometimes repetitively, especially after electrical stimulation of the cercal nerves. They were often in monosynaptic correlation with unitary EPSPs. 5. Neither the resting potential nor the postsynaptic membrane resistance was modified. 6. There were no changes in the equilibrium potentials of the ions involved in postsynaptic events. 7. The results may be essentially explained by an increase in transmitter release after 4-AP treatment, which may be partly the result of a rise in presynaptic terminal excitability, and partly the result of a lengthening of the presynaptic action potentials.     

Electrical Changes in Pre- and Postsynaptic Axons of the Giant Synapse of Loligo

Potential changes both in pre- and postsynaptic axons were recorded from the giant synapse of squid with intracellular electrodes. Synaptic current was also recorded by a voltage clamp method. Facilitation of postsynaptic potential caused by applying two stimuli several milliseconds apart was accompanied by an increase in the amplitude of the presynaptic action potential. Depression of the postsynaptic potential occurred without changes in the presynaptic action potential. Increase in the concentration of Ca in sea water caused an increase in amplitude of the synaptic current. On the other hand increase in Mg concentration decreased the amplitude of the synaptic current. In these cases no appreciable change in the presynaptic action potential was observed. Extracellularly recorded potential changes of the presynaptic axon showed mainly a positive deflexion at the synaptic region and a negative deflexion in the more proximal part of the presynaptic axon. Mechanism of synaptic transmission is discussed.     

Synaptic interactions between nonspiking local interneurones in the terminal abdominal ganglion of the crayfish

Nonspiking local interneurones are the important premotor elements in arthropod motor control systems. We have analyzed the synaptic interactions between nonspiking interneurones in the crayfish terminal (6th) abdominal ganglion using simultaneous intracellular recordings. Only 15% of nonspiking interneurones formed bi-directional excitatory connections. In 77% of connections, however, the nonspiking interneurones showed a one-way inhibitory interaction. In these cases, the presynaptic nonspiking interneurones received excitatory synaptic inputs from the sensory afferents innervating hairs on the surface of the uropods and the postsynaptic nonspiking interneurones received inhibitory synaptic inputs that were partly mediated by the inputs to the presynaptic nonspiking interneurones. The membrane hyperpolarization of the postsynaptic nonspiking interneurones mediated by the presynaptic nonspiking interneurones was reduced in amplitude when the hyperpolarizing current was injected into the postsynaptic interneurones, or when the external bathing solution was replaced with one containing low calcium and high magnesium concentrations. The role of these interactions in the circuits controlling the movements of the terminal appendages is discussed.Abbreviations AL antero-lateral - epsp excitatory postsynaptic potential - ipsp inhibitory postsynaptic potential - PL postero-lateral     

Electrophysiological investigation of the cat ciliary ganglion

Electrical responses of some nerves of the ciliary ganglion to stimulation of its other nerves were recorded, and intracellular recordings were also made from neurons of the ganglion (in situ). The overwhelming majority of preganglionic fibers terminate synaptically on neurons of the ganglion. Postganglionic fibers leave in the lateral and medial ciliary nerves, in which the velocity of conduction of excitation ranges from 1.9 to 9.0 m/sec. A few preganglionic fibers pass through the ciliary ganglion into the lateral ciliary nerve, giving off collaterals to neurons of the ganglion, so that stimulation of the lateral ciliary nerve evokes a response in the medial ciliary nerve (preganglionic axon reflex). The resting potential of neurons of the ciliary ganglion is 57±2.8 mV, and their action potential 68±3.6 mV. Single orthodromic stimulation usually evokes a single action potential in a neuron. The amplitude of the EPSP is increased during hyperpolarization of the postsynaptic membrane, confirming the chemical nature of synaptic transmission in the ganglion. The antidromic response consists of an IS-component and spike. The spike is followed by after-hyperpolarization, with a mean amplitude equal to 31% of the spike amplitude, and the time taken for it to fall to one–third of its initial amplitude is 75–135 msec.A. A. Bogomolets' Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 1, No. 1, pp. 101–108, July–August, 1969.     

Direction of action potential propagation influences calcium increases in distal dendrites of the cricket giant interneurons

To understand the relationship between the propagation direction of action potentials and dendritic Ca(2+) elevation, simultaneous measurements of intracellular Ca(2+) concentration ([Ca(2+)](i)) and intradendritic membrane potential were performed in the wind-sensitive giant interneurons of the cricket. The dendritic Ca(2+) transients induced by synaptically-evoked action potentials had larger amplitudes than those induced by backpropagating spikes evoked by antidromic stimulation. The amplitude of the [Ca(2+)](i) changes induced by antidromic stimuli combined with subthreshold synaptic stimulation was not different from that of the Ca(2+) increases evoked by the backpropagating spikes alone. This result means that the synaptically activated Ca(2+) release from intracellular stores does not contribute to enhancement of Ca(2+) elevation induced by backpropagating spikes. On the other hand, the synaptically evoked action potentials were also increased at distal dendrites in which the Ca(2+) elevation was enhanced. When the dendritic and axonal spikes were simultaneously recorded, the delay between dendritic spike and ascending axonal spike depended upon which side of the cercal nerves was stimulated. Further, dual intracellular recording at different dendritic branches illustrated that the dendritic spike at the branch arborizing on the stimulated side preceded the spike recorded at the other side of the dendrite. These results suggest that the spike-initiation site shifts depending on the location of the activated postsynaptic site. It is proposed that the difference of spike propagation manner could change the action potential waveform at the distal dendrite, and could produce synaptic activity-dependent Ca(2+) dynamics in the giant interneurons.     

Correlation of Transmitter Release with Membrane Properties of the Presynaptic Fiber of the Squid Giant Synapse

Depolarization of the presynaptic terminal by current produced a postsynaptic potential (PSP) which increased with increasing presynaptic polarization and then reached a plateau. Iontophoretic injection of tetraethylammonium ions (TEA) into the presynaptic axon near the terminal produced a prolonged presynaptic spike. The resulting PSP is increased in size and its time course closely followed that of the presynaptic spike. The presynaptic fiber no longer exhibited rectification and strong depolarizations revealed that the PSP reached a maximum with about 110 mv depolarization. Further depolarization produced a decrease in PSP amplitude and finally transmission was blocked. However, a PSP then always appeared on withdrawal of the depolarizing current. Under the conditions of these experiments, the PSP could be considered a direct measure of transmitter release. Bathing the TEA-injected synapse with concentrations of tetrodotoxin (TTX) sufficient to block spike activity in both pre- and postsynaptic axons did not greatly modify postsynaptic electrogenesis. However, doubling TTX concentration reversibly blocked PSP. Thus the permeability changes to Na and K accompanying the spike do not appear necessary for transmitter release. Some other processes related to the level of presynaptic polarization must be involved to explain the data. The inhibition of transmitter release by strong depolarizations appears to be related to Ca action. A membrane Ca current may also be necessary for normal transmitter release.     

Biophysical model of synaptic plasticity dynamics

We discuss a biophysical model of synaptic plasticity that provides a unified view of the outcomes of synaptic modification protocols, including: (1) prescribed time courses of postsynaptic intracellular Ca²⁺ release, (2) postsynaptic voltage clamping with presentation of presynaptic spike trains at various frequencies, (3) direct postsynaptic response to presynaptic spike trains at various frequencies, and (4) LTP/LTD as a response to precisely timed presynaptic and postsynaptic spikes.     

Mechanisms of direct and neural excitability in electroplaques of electric eel

1. Current flow outward through the caudal, reactive membrane of the cell causes direct stimulation of the electroplaque. The electrical response in denervated as well as in normal preparations recorded with internal microelectrodes is first local and graded with the intensity of the stimulus. When membrane depolarization reaches about 40 mv. a propagated, all-or-nothing spike develops. 2. Measured with internal microelectrodes the resting potential is 73 mv. and the spike 126 mv. The latter lasts about 2 msec. and is propagated at approximately 1 M.P.S. 3. The latency of the response decreases nearly to zero with strong direct stimulation and the entire cell may be activated nearly synchronously. 4. Current flow inward through the caudal membrane of the cell does not excite the latter directly, but activation of the innervated cell takes place through stimulation of the nerve terminals. This causes a response which has a latency of not less than 1.0 msec. and up to 2.4 msec. 5. The activity evoked by indirect stimulation or by a neural volley includes a prefatory potential which has properties different from the local response. This is a postsynaptic potential since it also develops in the excitable membrane which produces the local response and spike. 6. On stimulation of a nerve trunk the postsynaptic potential is produced everywhere in the caudal membrane, but is largest at the outer (skin) end of the cell. The spike is initiated in this region and is propagated at a slightly higher rate than is the directly elicited response. Strong neural stimulation can excite the entire cell to simultaneous discharge. 7. The postsynaptic potential caused by neural or indirect stimulation may be elicited while the cell is absolutely refractory to direct excitation. 8. The postsynaptic potential is not depressed by anodal, or enhanced by cathodal polarization. 9. It is therefore concluded that the postsynaptic potential represents a membrane response which is not electrically excitable. Neural activation of this therefore probably involves a chemical transmitter. 10. The nature of the transmitter is discussed and it is concluded that this is not closely related to acetylcholine. 11. Paired homosynaptic excitation discloses facilitation which is not present when the conditioning stimulus is direct or through a different nerve trunk. These results may be interpreted in the light of the existence of a neurally caused chemical transmitter or alternatively as due to presynaptic potentiation. 12. The electrically excitable system of the electroplaque has two components. In the normal cell a graded reaction of the membrane develops with increasing strength of stimulation until a critical level of depolarization, which is about 40 mv. 13. At this stage a regenerative explosive reaction of the membrane takes place which produces the all-or-nothing spike and propagation. 14. During early relative refractoriness or after poisoning with some drugs (eserine, etc.) the regenerative process is lost. The membrane response then may continue as a graded process, increasing proportionally to the stimulus strength. Although this pathway is capable of producing the full membrane potential the response is not propagated. 15. Propagation returns when the cell recovers its regenerative reaction and the all-or-nothing response is elicited. 16. Excitable tissues may be classified into three categories. The axon is everywhere electrically excitable. The skeletal muscle fiber is electrically excitable everywhere except at a restricted region (the end plate) which is only neurally or chemically excitable. The electroplaque of the eel, and probably also cells of the nervous system have neurally and electrically excitable membrane components intermingled. The electroplaques of Raia and probably also of Torpedo as well as frog muscle fibers of the "slow" system have membranes which are primarily neurally and chemically excitable. Existence of a category of invertebrate muscle fibers with graded electrical excitability is also considered. 17. In the eel electroplaque and also probably in the cells of neurons, tests of the mode of neural activation carried out by direct or antidromic stimulation cannot reveal the neurally and chemically activated component. The data of such tests though they appear to prove electrical transmission are therefore inadequate for the detection and study of the chemically initiated process.     

Mathematical formulations of Hebbian learning

 Several formulations of correlation-based Hebbian learning are reviewed. On the presynaptic side, activity is described either by a firing rate or by presynaptic spike arrival. The state of the postsynaptic neuron can be described by its membrane potential, its firing rate, or the timing of backpropagating action potentials (BPAPs). It is shown that all of the above formulations can be derived from the point of view of an expansion. In the absence of BPAPs, it is natural to correlate presynaptic spikes with the postsynaptic membrane potential. Time windows of spike-time-dependent plasticity arise naturally if the timing of postsynaptic spikes is available at the site of the synapse, as is the case in the presence of BPAPs. With an appropriate choice of parameters, Hebbian synaptic plasticity has intrinsic normalization properties that stabilizes postsynaptic firing rates and leads to subtractive weight normalization. Received: 1 February 2002 / Accepted: 28 March 2002 Correspondence to: W. Gerstner (e-mail: wulfram.gerstner@epfl.ch, Tel.: +41-21-6936713, Fax: +41-21-6935263)     

Radular mechanosensory neuron in the buccal ganglia of the terrestrial slug,Incilaria fruhstorferi

A radular mechanosensory neuron, RM, was identified in the buccal ganglia of Incilaria fruhstorferi. Fine neurites ramified bilaterally in the buccal ganglia, and main neurites entered the subradular epithelium via buccal nerve 3 (n3). When the radula was distorted by bending, RM produced an afferent spike which was preceded by an axonic spike recorded at n3. The response of RM to radular distortion was observed even in the absence of Ca²⁺, which drastically suppressed chemical synaptic interactions. Therefore, RM was concluded to be a primary radular mechanoreceptor.During rhythmic buccal motor activity induced by food or electrical stimulation of the cerebrobuccal connective, RM received excitatory input during the radular retraction phase. In the isolated buccal ganglia connected to the radula via n3s, the afferent spike, which had been evoked by electrical stimulation of the subradular epithelium, was broadened with the phasic excitatory input. Since the afferent spike was also broadened by current injection into the soma, depolarization due to the phasic input may have produced the spike broadening.Spike broadening was also observed during repetitive firing evoked by current injection. The amplitude of the excitatory postsynaptic potential in a follower neuron increased depending on the spike broadening of RM.Abbreviations CBC cerebrobuccal connective - EPSP excitatory postsynaptic potential - n1,n3 buccal nerves 1 and 3 - RBMA rhythmic buccal motor activity - RM radular mechanosensory neuron - SMT supramedian radular tensor neuron     

Computational Consequences of Temporally Asymmetric Learning Rules: I. Differential Hebbian Learning

Temporally asymetric learning rules governing plastic changes in synaptic efficacy have recently been identified in physiological studies. In these rules, the exact timing of pre- and postsynaptic spikes is critical to the induced change of synaptic efficacy. The temporal learning rules treated in this article are approximately antisymmetric; the synaptic efficacy is enhanced if the postsynaptic spike follows the presynaptic spike by a few milliseconds, but the efficacy is depressed if the postsynaptic spike precedes the presynaptic spike. The learning dynamics of this rule are studied using a stochastic model neuron receiving a set of serially delayed inputs. The average change of synaptic efficacy due to the temporally antisymmetric learning rule is shown to yield differential Hebbian learning. These results are demonstrated with both mathematical analyses and computer simulations, and connections with theories of classical conditioning are discussed.     

Statistical Analysis of Membrane Potential Fluctuations: Relation with Presynaptic Spike Train

In a study of integration at the single neuron level, the relationships between the postsynaptic membrane potential and the presynaptic spike train were analyzed. Fluctuations in membrane potential of neurons in the visceral ganglion of Aplysia were measured and described by histograms. The histogram estimates the probability density function of the membrane potential. Comparisons were made among histograms when there was no synaptic input, and when there was a single input in which variations were made in the PSP (postsynaptic potential) sign, i.e. excitatory or inhibitory, and arrival statistics, e.g. slow or fast, regular, Poisson-like, or patterned. This was examined in cells where the membrane potential was constant and in cells in which there was spontaneous pacemaker activity. The form of the histogram depended on whether the neuron was spontaneously quiescent or a pacemaker, or whether it received presynaptic input and, if it did, on the sign and temporal characteristics of such input. From such histograms the mean firing rate of output spike trains can be predicted; additional information of a temporal nature is required, however, to predict features of the interval structure of the output train. Suggestions are made concerning the way the nervous system might utilize the information summarized in the membrane potential histogram.     

Properties of synaptic noise in tonically active human motoneurons

The objective of these experiments was to determine the amount of synaptic noise on the cell membrane at various intervals after an action potential in a motoneuron firing at a specified frequency. Sources of noise such as variations in the level of voluntary drive were minimized by selecting only segments of the spike train in which the unit was running within prescribed frequency limits. The level of the membrane potential of the motoneuron during these intervals was determined using two test “pulses” (compound Ia excitatory postsynaptic potentials) of known amplitude. This enabled the probability of the membrane potential falling within a voltage “window” of known size at known times after the preceding spike to be determined. The probability density histograms showed that the fluctuations of membrane potential about a target interspike trajectory (i.e., the membrane noise) increased with time after the preceding spike. These fluctuations in the membrane potential can be accounted for by a one-dimensional “random walk” model of membrane noise. This model explains the salient features of the interval histograms, such as positive skewness at low target frequencies. A quantitative test of the model demonstrated its applicability to the motor pools of tibialis and masseter.