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Results for “Synaptic Transmission”

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At least 19 recordsLinked to original sources

PubMed1972

Adenosine 3',5'-monophosphate: electrophysiological evidence for a role in synaptic transmission.

Synaptic potentials and changes in resting membrane potentials of superior cervical ganglia of the rabbit were measured in the presence of adenosine 3',5'-monophosphate and agents that affect its metabolism. Adenosine 3',5'-monophosphate and its mono- and dibutyryl derivatives caused a hyperpolarization of the postganglionic neurons. Theophylline potentiated the slow inhibitory postsynaptic potential that follows synaptic transmission, as well as the hyperpolarization of postganglionic neurons caused by exogenous dopamine. Conversely, prostaglandin E(1) inhibited both the slow inhibitory postsynaptic potential and the dopamine-induced hyperpolarization. We hypothesize that the slow inhibitory postsynaptic potential as well as the dopamine-induced hyperpolarization result from increased amounts of adenosine 3'5'-monophosphate in the postganglionic neurons. The dibutyryl derivative of guanosine 3'5'-monophosphate caused a depolarization of the postganglionic neurons, which is consistent with the possibility that guanosine 3'5'-monophosphate mediates synaptic transmission at muscarinic cholinergic synapses.

Animals↗

PubMed1991

Enhanced synaptic transmission at identified synaptic connections in the cerebral ganglion of Aplysia.

The identified A-B neuron synaptic connections in the cerebral ganglion of Aplysia exhibited a novel form of enhanced synaptic transmission. A brief high-frequency train of action potentials (2 s, 10-30 Hz) in the presynaptic A neurons produced a long-lasting increase in the amplitude of excitatory postsynaptic potentials (EPSPs) in B neurons. The increase in synaptic efficacy was termed slow developing potentiation (SDP) since the EPSP amplitude increased slowly with the peak occurring 5 min after the tetanizing train. Peak EPSP amplitudes increased relative to the initial EPSP by an average of greater than 250%. SDP decayed as a single exponential with a time constant of tau = 24 min. The enhanced transmission was neuron specific. Only the connections made by the tetanized A neuron were potentiated. However, potentiation apparently occurred at all the synapses made by the tetanized A neuron. Tetanizing the postsynaptic B neurons neither induced, nor when paired with A neuron tetanization, increased SDP. SDP appears to be primarily due to increased transmitter release by the presynaptic neuron.

Action Potentials↗

PubMed1991

Modulation of synaptic transmission in the retina.

Synaptic transmission between photoreceptors and horizontal cells can be modulated in at least two domains: amplitude and time. In teleost fish, synaptic transmission is modulated mainly in the amplitude domain. Cone-driven horizontal cells in this species require background illumination to maintain high light responsiveness, and they are strongly suppressed in prolonged darkness. Moreover, in light, cone horizontal cells are extensively coupled via gap junctions, and the coupling is reduced in strength after prolonged darkness. The dopaminergic interplexiform cells play a major role in the regulation of cone horizontal cell activity. They may release dopamine tonically in darkness, which suppresses the light responsiveness of horizontal cells and uncouples them. In amphibians, whose horizontal cells receive input from both rods and cones, the modulation appears to be in the time domain, i.e., the rise time of horizontal cell responses is slow in prolonged darkness and accelerated after background illumination. gamma-aminobutyric acid and glycine may mediate the changes in response rise time. Despite the differences of the neuromodulators involved, these species provide two complementary modes of modulation of synaptic transmission in the retina.

Animals↗

PubMed1992

Neuronal excitability: voltage-dependent currents and synaptic transmission.

Neuronal membrane excitability and the synaptic connections among neurons produce behavior and cognition. The intracellular compartment of neurons is negatively charged relative to the extracellular space, and this charge, as well as current flow, is produced by ions. From the perspective of charged ions, the lipid bilayer of the neuronal membrane acts as a capacitor, and transmembrane glycoprotein pores or channels act as resistors. The open and closed states of ionic channels determine the membrane potential. At equilibrium, the lowest resistance or greatest permeability is for potassium, and the resting membrane potential is close to the equilibrium potential for potassium. When a channel is opened, permeable ions diffuse down their electrochemical gradients and the membrane potential is changed. Channels are gated (opened or closed) by voltage, neurotransmitters, and second messengers. The neuron integrates synaptic potentials produced by transmitter-gated channel activity and either generates a subthreshold potential, or a suprathreshold depolarization that generates an action potential or a burst of action potentials. Action potential generation is mediated by a large, brief sodium influx that is followed by activation of a voltage-dependent potassium eflux. The pattern of action potential firing is dependent on the interaction of a repertoire of voltage-dependent ion conductances. The action potential is the main signaling mechanism to activate synaptic transmission at axon terminals. Synaptic transmission is graded depending on the amount of calcium entering the presynaptic terminal. The number of action potentials, or the shape of the action potential, will determine the amount of calcium entering the terminal and the efficacy of synaptic transmission. Presynaptic ion channels may also be controlled by neurotransmitters or modulators and affect synaptic transmission by altering the amount of calcium influx.

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PubMed1989

Altered synaptic transmission in Drosophila hyperkinetic mutants.

Synaptic transmission in Drosophila can be altered by mutations in specific genes. For example, mutations in the Shaker (Sh) gene, which encodes the rapidly inactivating A-type potassium channel, cause repetitive nerve firing and prolonged transmitter release at the neuromuscular junction. Here we show that mutations in the Hyperkinetic (Hk) gene also affect the properties of synaptic transmission at the neuromuscular junction. In particular, we find that whereas single or low frequency nerve stimulation evokes a wild type postsynaptic response, at higher frequencies of nerve stimulation, each stimulus results in repetitive nerve firing and increased postsynaptic response, which is similar to that observed in Sh mutants. Various experiments suggest that this increased postsynaptic response results from prolonged depolarization of the nerve terminal, leading to increased transmitter release at the neuromuscular junction. The similarity in phenotypes between Sh and Hk mutants, along with the observation that Sh is epistatic to Hk in its effects on synaptic transmission, suggest that Hk acts on synaptic transmission by an effect on A-type potassium channels.

Animals↗

PubMedDate not supplied

Synaptic transmission in ammonia intoxication.

Ammonia intoxication allegedly plays a significant role in the pathophysiology of hepatic encephalopathy. In order to understand the pathogenesis of this encephalopathy it is necessary to know the effects of ammonia on the mechanisms by which neurons communicate, i.e., excitatory and inhibitory synaptic transmissions. NH4+ decreases excitatory synaptic transmission mediated by glutamate. Possibly, this effect is related to a depletion of glutamate in presynaptic terminals. NH4+ decreases inhibitory synaptic transmission mediated by hyperpolarizing Cl(-)-dependent inhibitory postsynaptic potentials. This effect is related to the inactivation of the extrusion of Cl- from neurons by NH4+. By the very same action, NH4+ also decreases the hyperpolarizing action of Ca2+- and voltage-dependent Cl- currents. These currents may modify the efficacy of the synaptic input to neurons and increase neuronal excitability. Estimates derived from experimental observations suggest that an increase of CNS tissue NH4+ to 0.5 mumol/g is sufficient to disturb excitatory and inhibitory synaptic transmission and to initiate the encephalopathy related to acute ammonia intoxication. Chronic portasystemic shunting of blood, as in hepatic encephalopathy, significantly changes the relation between CNS NH4+ and function of synaptic transmission. A portacaval shunt increases the tissue NH4+ necessary to disturb synaptic transmission. However, after a portasystemic shunt, synaptic transmission becomes extremely sensitive to any acute increase of NH4+ in the CNS.

Ammonia↗

PubMed1987

The probabilistic nature of synaptic transmission at a mammalian excitatory central synapse.

The synaptic connection between single group I afferents and dorsal spinocerebellar tract (DSCT) neurons in the cat spinal cord has been studied in an attempt to gain insight into the mechanisms of excitatory synaptic transmission in the mammalian CNS. Fluctuations in the amplitude of single group I fiber EPSPs in DSCT neurons were examined using a numerical deconvolution procedure to reduce the effects of contaminating noise. In general, it was found that single fiber EPSPs fluctuate in peak amplitude between discrete levels separated by equal or quantal increments. Many previous studies have proposed simple binomial statistics as a general model of quantal synaptic transmission. In the present study we show that simple binomial statistics do not describe the fluctuations in amplitude of single group I fiber EPSPs in DSCT neurons. It is suggested that nonuniformities in the probability of transmitter release from release site to release site explain the failure of the binomial model to describe the EPSP fluctuation pattern at this synapse. Nonuniform quantal transmission is proposed as a more adequate description of excitatory synaptic transmission in the mammalian CNS.

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PubMed1992

Characteristics of synaptic transmission in reinnervating rat skeletal muscle.

Synaptic transmission, and its sensitivity to the effects of 3,4-diaminopyridine (3,4-DAP) and the phosphatase 2,3-butanedione monoxime (BDM), was examined for "crushed fiber" preparations of rat extensor digitorum longus muscle undergoing reinnervation after nerve crush. While mean quantal content (m) of endplate potentials (EPPs) was low early during reinnervation (10-24 days after nerve crush), elevation of temperature or extracellular calcium concentration restored m toward normal. However, m achieved control values for reinnervating preparations exposed to 3,4-DAP. 3,4-DAP also activated quiescent motor nerve terminals: after exposure to this drug, synaptic transmission was detected as early as 8 days after nerve crush. BDM too activated quiescent regenerating motor nerve terminals and increased m to normal. It also prolonged EPP and endplate current decay, suggesting a pre-synaptic effect on the synchrony of transmitter release and/or a post-synaptic effect on the open time of acetylcholine-gated endplate channels. While the effects of temperature, extracellular calcium, 3,4-DAP, and BDM suggest that regenerating nerve terminals can mobilise a reserve of quanta, this reserve is abnormally low, since hemicholinium-3 caused rapid rundown of EPP amplitude at repetitively stimulated regenerating endplates.

4-Aminopyridine↗

PubMed1990

Aminergic modulation of graded synaptic transmission in the lobster stomatogastric ganglion.

Graded chemical synaptic transmission is important for establishing the motor patterns produced by the pyloric central pattern generator (CPG) circuit of the lobster stomatogastric ganglion (Raper, 1979; Anderson and Barker, 1981; Graubard et al., 1983). We examined the modulatory effects of the amines dopamine (DA), serotonin (5-HT), and octopamine (Oct) on graded synaptic transmission at all the central chemical synapses made by the pyloric dilator (PD) neuron onto its follower cells, using synaptic input-output curves measured from cell somata. DA strongly reduced the graded synaptic strength at all the PD synapses. DA reduction of chemical synaptic strength from PD onto the inferior cardiac (IC) neuron could change the sign of synaptic interaction between these 2 cells from inhibitory to excitatory by uncovering a weak electrical connection. 5-HT had weaker and more variable effects, reducing graded synaptic strength from the PD onto the lateral pyloric and pyloric neurons and enhancing the weak synapse from the PD to the IC cell. Oct strongly enhanced the graded synaptic strength at all the PD central synapses. Oct enhancement of graded synaptic strength between the PD and IC cells could also change the sign of the interaction: weak, excitatory electrical coupling, which was sometimes dominant before Oct, was masked by the enhanced chemical inhibitory interaction during Oct application. Measurements of electrical coupling between 2 PD cells and between 2 postsynaptic cells suggest that Oct does not change the input resistance of these cells and may act directly at the PD synapses. The effects of DA and 5-HT are most easily explained by their general reductions in pre- and postsynaptic input resistance. DA, 5-HT, and Oct each produce a distinct pyloric motor pattern (Flamm and Harris-Warrick, 1986a). These amine-induced motor patterns may be explained by the unique actions of each amine on the intrinsic membrane properties of different pyloric CPG neurons (Flamm and Harris-Warrick, 1986b) and by modulation of graded synaptic transmission between the pyloric neurons.

Action Potentials↗

PubMed1976

Calcium dependency of excitatory chemical synaptic transmission in the frog cerebellum in vitro.

Chemical synaptic transmission was studied with microelectrode techniques in isolated frog cerebella maintained in vitro. Purkinje cell (PC) EPSPs, elicited by selective monosynaptic electrical stimulation of both the parallel fiber (PF) and climbing fiber (CF) inputs, could be inverted by depolarizing (outward) current injections. Evoked synaptic transmission at both junctions was reduced by lowering the extracellular concentration of calcium ions ([Ca2+]) below 2 mM. Raising [Ca2+] above 2 mM to 8 mM did not further increase synaptic transmission. Mg2+, Sr2+, and Ba2+ did not substitute for Ca2+ in the transmission process.

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PubMed1990

Mechanism of action of local anesthetics on synaptic transmission in the rat.

The mechanism of action of local anesthetics on synaptic transmission and their effects on synaptic components and on electrophysiologic properties of the nerve cell body are not clear. Therefore, the effects of lidocaine and bupivacaine on pre- and postsynaptic mechanisms underlying synaptic transmission in sympathetic ganglia were studied utilizing the techniques of intracellular recording and stimulation on isolated superfused superior cervical ganglia of rats. Lidocaine and bupivacaine either depressed or completely blocked synaptic transmission in sympathetic ganglia in a dose-dependent manner. Blockade of axonal conduction in presynaptic fibers was preceded by increased latency (the latency increased from 11.2 +/- 0.9 to 16.5 +/- 1.4 ms, mean +/- SEM, P less than 0.01) when the drugs were applied to the presynaptic nerves. Application of the drugs directly to the ganglion produced alterations in postsynaptic membrane properties consisting of decreased membrane resistance (from 40 +/- 3 to 32 +/- 3 M omega, P less than 0.01), increased firing threshold (from 14 +/- 0.5 to 18 +/- 0.5 mV, P less than 0.01), and decreased action potential amplitude (P less than 0.01) and/or blockade of action potential generation. Resting postsynaptic membrane potential did not change significantly. These changes were reversible. However, even after the excitatory postsynaptic potential resulting from presynaptic nerve stimulation had fully recovered during washout of the local anesthetic, the threshold for evoking the spike potential (firing level) still remained elevated for both presynaptic and intracellular stimulation of the ganglion cell, suggesting prolonged cell depression.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1990

Role of NMDA and non-NMDA receptors in synaptic transmission in rat piriform cortex.

The pharmacology of synaptic transmission was studied in slices of rat piriform cortex using the selective non-NMDA glutamate receptor antagonist 6.7-dinitroquinoxaline-2,3-dione (DNQX) and the selective NMDA receptor antagonist D-2-amino-5-phosphonopentanoate (D-AP5). DNQX produced a dose-dependent blockade of synaptic transmission at both lateral olfactory tract and associational system synapses with half-maximal effects at about 2.5 microM. D-AP5 had no significant effects on field potentials recorded in medium containing 2.5 mM Mg++. However in low Mg++ (100-200 microM) medium, D-AP5 did reduce a slow component of postsynaptic responses in both synaptic systems. In Mg(++)-free medium, 20 microM DNQX did not completely block transmission; the remaining response components were blocked by D-AP5. These results suggest that normal synaptic transmission in the two main inputs to the superficial layers of piriform cortex is mediated by non-NMDA receptors but that NMDA receptors can also participate under conditions where the Mg++ block of the NMDA channel is alleviated.

2-Amino-5-phosphonovalerate↗

PubMed1991

Effects of axotomy on synaptic transmission and structure in frog sympathetic ganglia.

Axotomy was carried out on frog sympathetic neurons of the two last lumbar chain ganglia. At different times thereafter, synaptic transmission was analysed electrophysiologically by intracellular microelectrodes and compared with synaptic density, measured by electron microscopy in the same ganglia. For this purpose, modifications in synaptic transmission were estimated first, by the numbers of B and C sympathetic neurons exhibiting subthreshold excitatory postsynaptic potentials in response to 10 Hz orthodromic stimulation of preganglionic fibres, and second, by the amplitude and number of excitatory postsynaptic potentials occurring over 5-10 s periods of 10 Hz stimulation. By distinguishing two types of morphological relationships between the pre- and postsynaptic elements, two contact indices were defined: a synaptic index (ratio of the number of synapses encountered to the number of perikarya explored) and a simple contact index corresponding to the same type of contacts, but without any membrane differentiation. Both the electrophysiological and morphological results showed that the first effects were detectable 4 days after axotomy, and that the main alterations in synaptic transmission and density occurred at 2 weeks. In addition, while in normal ganglia the excitatory postsynaptic potentials of B and C neurons reached the threshold for action potential generation in response to 10 Hz stimulation, about 29% of the axotomized neurons had subthreshold excitatory postsynaptic potentials 1 week after section. At 2 weeks, this proportion reached 65%, and the synaptic and simple contact indices, at 90% and 60% respectively, were significantly lower than the control ganglion indices. At longer times after axotomy, there was a discrepancy between the morphological and electrophysiological results: at 1 month, the synaptic index seemed to rise as the decline in the efficacy of synaptic transmission became more marked. The amplitude of the subthreshold excitatory postsynaptic potentials recorded in B neurons was 5.5 +/- 2.8 mV (mean +/- SD, n = 18); this value was significantly lower by about 50% than that measured 1 week after axotomy. In addition, the number of excitatory postsynaptic potentials in B neurons reached an average maximum of 83 +/- 29 for 100 stimuli applied at 10 Hz. Similar results were obtained for C neurons. Two months after axotomy, the physiological and morphological parameters of synaptic efficacy began to recover and return to normal values, but had not reached them by 4 months. These observations show that some synaptic transmission remains possible, even with a much reduced number of synaptic complexes. It is suggested that after axotomy, simple contacts also might be involved in synaptic transmission.

Animals↗

PubMed1990

Neurochemical and electrophysiological studies on the inhibitory effect of ammonium ions on synaptic transmission in slices of rat hippocampus: evidence for a postsynaptic action.

To elucidate the mechanisms involved in the inhibition of synaptic transmission by ammonium ions, the effects of NH4Cl on glutamate release and on synaptic transmission from Schaffer collaterals to CA1 pyramidal cells were measured in fully submerged slices of rat hippocampus. The large, Ca(2+)-dependent release of glutamate evoked by electrical-field stimulation or by 56 mM K+ was not reduced by 5 mM NH4Cl. In contrast, 5 mM NH4Cl decreased the smaller, field stimulation-induced release of glutamate observed in the presence of low concentrations of Ca2+ (0.1 mM), as well as the spontaneous release of glutamate both in normal and low Ca2+. Unlike the Ca(2+)-dependent release of glutamate, synaptic transmission was reversibly depressed even by 1 mM NH4 Cl. Firing of CA1 pyramidal cells evoked by iontophoretically applied glutamate was significantly inhibited by 2 or 5 mM NH4Cl. This depression was increased in the presence of 25 microM bicuculline. Results suggest that ammonium ions do not depress the Ca(2+)-dependent release of glutamate originating from synaptic vesicles, which is involved in synaptic transmission. Rather, ammonium ions inhibit synaptic transmission by a postsynaptic action, a conclusion strengthened by the inhibitory effect of NH4Cl on glutamate-induced firing. However, NH4Cl may inhibit the formation of cytoplasmic glutamate, the source of spontaneous and Ca(2+)-independent release.

Amino Acids↗

PubMed1985

[Effect of chemical carcinogens on the synaptic transmission of excitation in the sympathetic ganglia of rats].

Acute experiments on rats were performed to study the influence of water-soluble chemical carcinogens on synaptic transmission via the inferior mesenteric sympathetic ganglion. Synaptic transmission was studied before and after intravenous injection of the enterotropic carcinogen 1,2-dimethylhydrazine (DMH) and N-nitrosomethylurea (NMU) which induces the development of mammary gland tumors. Despite the different chemical structure and specificity of the action of the carcinogens used on one or another target tissue, their influence on synaptic transmission via the sympathetic ganglia was of identical character, manifested by the blocking action on transmission of nerve impulses. Comparison of the action of DMH and NMU on synaptic transmission with the influence of some other pharmacological substances suggests that the mechanism of the inhibitory action of the carcinogens on synaptic transmission via the sympathetic ganglia may be linked both with cholinolytic and adrenomimetic influences of the carcinogens.

Action Potentials↗

PubMed1989

Ammonium decreases excitatory synaptic transmission in cat spinal cord in vivo.

1. Glutamine is thought to be a precursor of the pool of glutamate that is used as synaptic transmitter. NH4+ inhibits glutaminase, the enzyme presumed to cleave glutamine into glutamate in synaptic terminals. Therefore a decrease by NH4+ of excitatory synaptic transmission in hippocampus was suggested to be due to the inability to utilize glutamine as a precursor for glutamate and subsequent transmitter depletion. This study reexamines the effects of NH4+ on excitatory synaptic transmission. 2. The effects of NH4+ on excitatory synaptic transmission from low-threshold afferent fibers, presumably Ia-afferent fibers, to motoneurons was investigated in the spinal cord of anesthetized cats in vivo. 3. Action potentials of low-threshold afferent fibers were recorded at the entry of the dorsal roots into the spinal cord. An extracellular electrode within a motoneuron nucleus recorded the action potential of low-threshold afferent fibers and the extracellular monosynaptic excitatory postsynaptic potential, i.e., the focal synaptic potential (FSP). This extracellular electrode also recorded the antidromic field potential (AFP) in response to ventral root stimulation. Electrodes on the ventral roots recorded the monosynaptic reflex (MSR) and the monosynaptic excitatory postsynaptic potential in motoneurons electrotonically conducted into the ventral roots (VR-EPSP). 4. Intravenous infusion of ammonium acetate (AA) reversibly decreased MSR, VR-EPSP, and FSP, i.e., decreased excitatory synaptic transmission. 5. The decrease of VR-EPSP and FSP was accompanied initially by a decrease of conduction and, eventually, a conduction block in presynaptic terminals of low-threshold afferent fibers. 6. The decreases of VR-EPSP and FSP were also accompanied by the transient appearance of a reflex discharge, triggered by VR-EPSPs of decreased amplitude, and changes of the AFP indicating increased invasion of motoneuron somata by antidromic action potentials. 7. It is suggested that NH4+ depolarizes intraspinal Ia-afferent fibers and motoneurons. This depolarization initially decreases and then blocks conduction of action potentials into the presynaptic terminals of Ia-afferent fibers. The conduction block prevents the release of excitatory transmitter and decreases excitatory synaptic transmission. 8. The suggested depolarizing action of NH4+ may be due to K+-like ionic properties of NH4+ and/or an inhibition of K+-uptake into astrocytes. 9. The conduction block in presynaptic terminals of low-threshold afferent fibers can fully explain the decrease of excitatory synaptic transmission by NH4+. Because of the conduction block in presynaptic terminals, this study does not permit a conclusion as to an inhibition by NH4+ fo the utilization of glutamine as a precursor for glutamate used as synaptic transmitter.

Action Potentials↗

PubMed1991

Synaptic formations and modulations of synaptic transmissions between identified cerebellar neurons in culture.

1. Synaptic formations between a rat cerebellar granule cell and a Purkinje cell, and also between an inferior-olivary neuron and a Purkinje cell have been accomplished in culture. 2. The synaptic transmission between an inferior-olivary neuron and a Purkinje cell was far much more potent than that between a granule cell and a Purkinje cell in the culture, and the former always induced in a Purkinje cell an action potential followed by prolonged depolarization, which resembled a climbing fiber response in vivo. 3. Synaptic potentiation was induced by repetitive stimulation (2 Hz, 20 sec) of a granule cell, and the synaptic depression was induced by repetitive conjunctive stimulation of both a granule cell and an inferior-olivary neuron as in a slice preparation. 4. When repetitive stimulation of both neurons were given while the postsynaptic Purkinje cell was voltage-clamped at -80 mV, not the depression but the potentiation took place. When repetitive stimulation of a granule cell was coupled with the postsynaptic strong depolarization induced by direct outward current injection, the depression took place. These two experiments indicate that the postsynaptic depolarization during activation of a presynaptic granule cell is both necessary and sufficient to induce the depression, and that the potentiation is induced without the postsynaptic depolarization. 5. The quantal analysis on the synaptic transmission, where fluctuations of amplitudes of synaptic currents in a Purkinje cell induced by a single granule cell were measured, indicated that the synaptic potentiation involves the enhancement of transmitter release from a presynaptic granule cell and that the depression involves changes of postsynaptic receptors on a Purkinje cell.

Animals↗

PubMed1977

The analysis of nonlinear synaptic transmission.

In order to characterize synaptic transmission at a unitary facilitating synapse in the lobster cardiac ganglion, a new nonlinear systems analysis technique for discrete-input systems was developed and applied. From the output of the postsynaptic cell in response to randomly occurring presynaptic nerve impulses, a set of kernels, analogous to Wiener kernels, was computed. The kernels up to third order served to characterize, with reasonable accuracy, the input-output properties of the synapse. A mathematical model of the synapse was also tested with a random impulse train and model predictions were compared with experimental synaptic output. Although the model proved to be even more accurate overall than the kernel characterization, there were slight but consistent errors in the model's performance. These were also reflected as differences between model and experimental kernels. It is concluded that a random train analysis provides a comprehensive and objective comparison between model and experiment and automatically provides an arbitrarily accurate characterization of a system's input-output behavior, even in complicated cases where other approaches are impractical.

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