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At least 19 recordsLinked to original sources
PubMed1992

Statistical analysis of long-term potentiation of large excitatory postsynaptic potentials recorded in guinea pig hippocampal slices: binomial model.

Excitatory postsynaptic potentials (EPSPs) were recorded in guinea pig hippocampal slices (area CA1) from 15 neurons after stimulation of stratum radiatum (str. rad.) and stratum oriens. EPSP amplitudes increased in 8 neurones (10 post-tetanic regions) recorded 15 to 45 min after tetanic stimulation of str. rad. The increase was considered to represent long-term potentiation (LTP). Quantal analysis was performed by two methods assuming binomial statistics: the histogram method using deconvolution of noise and the variance method. According to both methods, LTP was associated with an increase in mean quantal content (m) which correlated with LTP magnitude. A statistically significant increase in quantal size (v) was found only by the histogram method and the increase was not correlated with LTP magnitude. A separate analysis of EPSPs with small LTP magnitude demonstrated that with the histogram method only v was increased but not m. A smaller increase in m for the pooled data of both methods did not correlate with LTP magnitude for this EPSP subset. The increase in m for the whole EPSP set corresponds to previous results on the quantal analysis of LTP in in vivo preparations and favours a presynaptic location of major mechanisms underlying LTP maintenance. The increase in v indicates the existence of another mechanism responsible for the maintenance of a small part of LTP. This mechanism might involve either pre- or postsynaptic changes or both.

Algorithms↗
PubMed1992

Quantal analysis of long-term potentiation of "minimal" excitatory postsynaptic potentials in guinea pig hippocampal slices: binomial approach.

"Minimal" excitatory postsynaptic potentials (EPSPs) were recorded from 13 neurones in area CA1 of guinea pig hippocampal slices after double-pulse stimulation of stratum radiatum (str. rad.) and stratum oriens (str. or.). Amplitudes of EPSPs significantly increased in 8 neurones 5 to 55 min after 9 tetanizations in str. rad.. The increase was considered to represent long-term potentiation (LTP). Altogether 26 EPSPs (42 post-tetanic regions) were statistically analysed by four methods of the quantum hypothesis assuming the binomial model of transmitter release: the deconvolution (histogram), the variance, the failures, and the combined (variance-failures) methods. The mean quantal content (m) significantly increased after LTP induction according to all methods used. Quantal size (v) also tended to increase but according to some methods, the increase was not statistically significant and it did not correlate with LTP magnitude. However, for an EPSP subset with a LTP magnitude of less than 1.55, the increase in v correlated with LTP magnitude, whereas the increase in m did not. The relative contribution of the increase in v to LTP magnitude was larger for cases with small LTP than for the whole EPSP set. In general, the increase in m corresponds to previous studies and favours the presynaptic location of major mechanisms of LTP maintenance, i.e. an increase in the average number of transmitter quanta released by each presynaptic volley. The post-tetanic increase in v might reflect some additional mechanisms which presumably include an increase in the amount of transmitter in one quantum.

Animals↗
PubMed1989

Influences of morphology and topography of motoneurons and muscle spindle afferents on amplitude of single fiber excitatory postsynaptic potentials in cat.

Excitatory postsynaptic potentials (e.p.s. p.s.) elicited by impulses in single muscle spindle afferent fibers from the medial gastrocnemius (m.g.) muscle were recorded intracellularly from homonymous and heteronymous motoneurons in order to study factors that influence the amplitudes of such responses. Impulses in large afferent fibers elicited larger single-fiber e.p.s.p.s. than those in smaller afferents. Mean e.p.s.p. amplitudes were related exponentially to afferent conduction velocities of both Ia and spindle group II fibers. The closer a motoneuron was to the spinal entry point of an afferent fiber, the larger was the mean e.p.s.p. amplitude evoked in it. Impulses in the same afferent fiber elicited larger e.p.s.p.s in small than large motoneurons when the two cells were located at the same craniocaudal levels. Other factors being equal, the single-fiber e.p.s.p.s evoked in homonymous and heteronymous motoneurons were approximately equal in amplitude. Relatively simple morphological and topographical explanations for the findings were advanced and their functional significance for orderly recruitment in partitioned and unpartitioned reflexes was described.

Action Potentials↗
PubMed1989

Fast hyperpolarization following an excitatory postsynaptic potential in cat bladder parasympathetic neurons.

Intracellular recording techniques were used to study a fast hyperpolarizing potential following the fast excitatory postsynaptic potential evoked by an orthodromic nerve stimulation in cat bladder parasympathetic ganglion cells. In the 61 ganglion cells examined, two types of responses were recorded on stimulating the preganglionic nerve; one had only a fast excitatory postsynaptic potential (type SI, n = 20) and the other had a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential (type SII, n = 41). In type SII neurons, the half-maximum duration of the afterhyperpolarizing potential following an orthodromic spike was longer than that of a direct spike produced by injecting a depolarizing current pulse through the recording electrode; the half-maximum durations for afterhyperpolarizing potentials following orthodromic and direct action potentials were comparable in type SI cells. Blocking the initiation of an orthodromic spike by hyperpolarizing the membrane in type SII cells revealed a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential which was similar to that observed at the resting potential. The fast hyperpolarizing potential had a duration comparable to that of an afterhyperpolarizing potential following an orthodromic action potential. The fast excitatory postsynaptic potential-fast hyperpolarizing potential sequence was blocked completely and reversibly by nicotinic receptor antagonists (hexamethonium and D-tubocurarine). Atropine, alpha-2 noradrenergic (yohimbine and phentolamine), and purinergic (caffeine) antagonists had no effect on the fast hyperpolarizing potential. In cells which show type SII responses, spontaneous excitatory postsynaptic potentials were not followed by a hyperpolarization. Depolarizing the membrane (by passing a cathodal current through the recording electrode) to an amplitude comparable to that of a fast excitatory postsynaptic potential also did not elicit a membrane hyperpolarization in type SII cells. In some cells, stimulating one preganglionic nerve trunk elicited a fast hyperpolarizing potential, but activating another nerve trunk innervating the same ganglion cell did not. There was no correlation between the variations in the amplitudes of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential in type SII cells, but increasing the stimulus intensity applied to the presynaptic nerve fiber potentiated the amplitude of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential. The fast hyperpolarizing potential was not associated with appreciable changes in input resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1990

Changes in field excitatory postsynaptic potential shape induced by tetanization in the CA1 region of the guinea-pig hippocampal slice.

The present paper contains a description of a prolonged potentiation of the field excitatory postsynaptic potential in the CA1 region of the hippocampal slice preparation following afferent tetanization. In contrast to long-term potentiation, this novel potentiation is not specific to the activated synapses, and manifests itself as a change in the shape of the field excitatory postsynaptic potential with a prolongation of the rising phase and an increased peak amplitude. The potentiation is fully developed within minutes after tetanization and shows no decrement for at least an hour. Although it can appear together with long-term potentiation following tetanization at moderate strength (single volley excitatory postsynaptic potential below threshold for spike initiation), it is more readily seen following tetanization at higher strengths. The N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonovalerate prevents the induction but not the maintenance of the shape modification. The potentiation is observed in the presence of the GABAA antagonist picrotoxin (100 microM) and is thus not secondary to changes in postsynaptic inhibition. 4-Aminopyridine (50-100 microM) produced changes in the field excitatory postsynaptic potential resembling the shape modification produced by afferent tetanization, suggesting that the potentiation may be due to a blockade of potassium channels, pre- or postsynaptically located. The potentiation is also found to be associated with an increase in the population spike for a given initial slope of the field excitatory postsynaptic potential, and may thus contribute to the excitatory postsynaptic potential-spike potentiation that can be observed following afferent tetanization.

2-Amino-5-phosphonovalerate↗
PubMed1992

Fast excitatory postsynaptic potentials and the responses to excitant amino acids of sympathetic preganglionic neurons in the slice of the cat spinal cord.

The properties of the excitatory postsynaptic potential evoked by focal stimulation and of the responses to excitatory amino acids were examined by intracellular recording from sympathetic preganglionic neurons in upper thoracic spinal cord slices of the adult cat. Single stimuli to the region dorsal to the intermedio-lateral nucleus evoked short-latency, presumably monosynaptic, excitatory postsynaptic potentials. The reversal potential of this response was -2.2 mV and became more negative when external Na+ or K+ concentration was decreased. The excitatory postsynaptic potential was depressed by the non-selective excitatory amino acid receptor antagonist cis-2,3-piperidine dicarboxylic acid and enhanced by a glutamate uptake inhibitor. The non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2.3-dione abolished the excitatory postsynaptic potential in 72% of neurons. In the remaining neurons, this antagonist only depressed the potential and unmasked a slower component which was abolished by the N-methyl-D-aspartate receptor antagonist D,L-2-amino-5-phosphonovaleric acid. In the presence of tetrodotoxin all neurons tested were depolarized by glutamate or aspartate, as well as by the selective agonists quisqualate, alpha-amino-3-hydroxy-5-methylisoxazole propionic acid, kainate and N-methyl-D-aspartate. The glutamate-evoked depolarization reversed at a membrane potential of -2.0 mV and at a more negative value when external Na+ or K+ concentration was decreased. The response to alpha-amino-3-hydroxy-5-methylisoxazole propionic acid was abolished by 6-cyano-7-nitroquinoxaline-2,3-dione in all neurons tested and that to kainate in only one-third of the cells. In the remainder the response to kainate was only slightly depressed by this antagonist. The responses to glutamate and aspartate were only slightly depressed by the combined action of the various amino acid receptor antagonists used. The responses to N-methyl-D-aspartate were abolished by D,L-2-amino-5-phosphonovaleric acid. The punched-out region of the intermedio-lateral nucleus, maintained in vitro, released glutamate and aspartate in the absence of stimulation. Field stimulation (20 Hz) enhanced release by between 40 and 100%. The increase was prevented by superfusion with calcium-free Krebs. It is concluded that excitatory amino acids, acting on both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors, but mainly on the latter, are likely mediators of the monosynaptic excitatory postsynaptic potential evoked in sympathetic preganglionic neurons by the stimulated region. The efflux data suggest that glutamate and aspartate are among the mediators.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1988

Voltage-clamp analysis of taurine-induced suppression of excitatory postsynaptic potentials in frog spinal motoneurons.

1. The depressant actions of taurine applications on lumbar motoneurons in the isolated frog spinal cord were studied using conventional intracellular recordings and the two-electrode voltage-clamp technique. 2. With microelectrodes containing K+-acetate, 0.75-2 mM taurine mostly induced a hyperpolarization that often faded or turned into depolarization during the continuous application. A higher concentration (5-7.5 mM) depolarized a majority of cells. The effects on the membrane potential were associated with an increase in input conductance (approximately 285%). 3. The reversal potential of the taurine-induced currents was approximately -70 mV, with microelectrodes containing K+-acetate. In recordings using KCl-filled electrodes, taurine (less than or equal to 2 mM) produced a large depolarization (greater than or equal to 20 mV) at resting potentials near -50 mV, thereby indicating that the reversal potential was positively shifted by loading the cell with Cl-. These results suggest that the taurine potentials were mediated predominantly by an increased Cl- permeability. 4. Voltage-dependent relaxations of taurine currents were observed in 10 of 14 neurons. 5. A linear relation was found between the input conductance and the amount of current required to generate a 1-mV increment in EPSP at resting potential. 6. Polysynaptic excitatory postsynaptic potentials (EPSPs) and currents (EPSCs) were more susceptible to taurine than the monosynaptic responses. Taurine (less than 1 mM) seemed to suppress the interneurons mediating polysynaptic pathways. 7. Monosynaptic EPSPs and EPSCs were decreased with higher concentrations of taurine (greater than 1 mM). The percent reduction of EPSPs and that of the corresponding EPSCs had a positive correlation (r = 0.95), whereas, there was no significant correlation between changes in EPSPs and in input conductance, and between changes in EPSCs and in input conductance. The amount of current required to produce a 1-mV increment of EPSP was increased in the presence of taurine, in association with the increased input conductance. 8. Taurine suppressed synaptic potentiation of EPSPs evoked by paired stimuli, at an interval of 60-180 ms. Gamma-D-glutamylglycine, an antagonist of receptors for excitatory amino acids, greatly reduced the amplitude of EPSPs, but had little effect on synaptic potentiation. 9. Taurine suppressed glutamate currents evoked at membrane potentials, clamped near rest in low Ca2+, high Mg2+ solution. 10. These findings suggest that the taurine-induced reduction of EPSPs is due mainly to suppression of EPSCs, through both presynaptic and postsynaptic mechanisms.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Voltage dependence of excitatory postsynaptic potentials of rat neocortical neurons.

1. The properties of excitatory postsynaptic potentials (EPSPs) of rat neocortical neurons were investigated with a fast single-electrode current-voltage clamp in vitro. Typically, apparently pure EPSPs were obtained by selection of electric stimuli of low intensity. 2. The amplitude and time integral of the EPSP increased when the neuron was depolarized. At threshold for generation of action potentials, the amplitude of EPSPs was increased by approximately 30% [from 5.0 +/- 2.1 to 6.3 +/- 1.0 (SD) mV, n = 12]. The integral of EPSPs was maximally about fourfold (3.7 +/- 1.5, n = 16) larger than at resting membrane potential (Em). The mechanisms involved in this augmentation of EPSPs were further investigated. 3. The amplitude and the time integral of excitatory postsynaptic currents (EPSCs) decreased linearly with shifts in command potential from -100 to -60 mV. The decrease of the EPSC integral with depolarization indicates that the enhancement of the EPSP may be brought about by recruitment of a voltage-dependent inward current. 4. Evoking EPSPs at various delays after the onset of small depolarizing current pulses (0.3-0.6 nA, 600 ms) revealed that augmentation decays with time. The integral of EPSPs evoked approximately 80 ms after the onset of the current pulse was 3.7 (+/- 1.5, n = 16) times larger than at Em. The integral of EPSPs evoked at 480 ms. however, were only twofold (+/- 0.7, n = 16) larger. Hence EPSPs evoked after a delay of 80 ms were 1.7-fold (+/- 0.4, n = 24) larger than EPSPs evoked after 480 ms. EPSCs were independent of the delay of stimulation at all potentials. 5. Intracellular application of the lidocaine derivative N-(2,6-dimethyl-phenylcarbamoylmethyl) triethylammonium bromide (QX 314) at 100 mM from pipettes rapidly abolished fast action potentials and inward rectification. During comparable depolarizations the increase in EPSP integrals was much smaller in QX 314-treated neurons than in controls. On average, the integral of EPSPs evoked at 70-90 ms was 1.7 times (+/- 1.0) larger than at Em, and the integral of EPSPs evoked with larger delays was close to the value obtained at resting Em (0.9 +/- 0.3, n = 8). The ratio of EPSP integrals early versus late (1.8 +/- 0.5) is comparable to controls, suggesting that QX 314-sensitive currents are unlikely to be involved in the time-dependent enhancement. 6. Mimicking EPSPs by brief depolarizations atop long depolarizations revealed a time- and voltage-dependent enhancement comparable to that of EPSPs.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1973

Pentobarbital: selective depression of excitatory postsynaptic potentials.

The effects of pentobarbital (Nembutal) on synaptic transmission and postsynaptic potentials were studied by the use of several invertebrate preparations. Pentobarbital selectively and reversibly depressed both excitatory postsynaptic potentials and sodium-dependent postsynaptic responses to putative excitatory transmitters without affecting either inhibitory postsynaptic potentials or chloride- and potassium-dependent postsynaptic responses to putative transmitters. A selective depression of postsynaptic excitatory events was also observed with other central nervous system depressants (ethanol, chloroform, chloralose, diphenylhydantoin, and urethane). The results suggest that central and peripheral depression observed during general anesthesia is due to a selective depression of excitatory synaptic events.

Acetylcholine↗
PubMed1989

Simultaneous recording of presynaptic spikes and excitatory postsynaptic potentials from monosynaptically connected hippocampal neurons.

A technique has been devised to activate single granule cells in the hippocampus, and to record simultaneously spikes from the particular granule cell and excitatory postsynaptic potentials from a monosynaptically connected CA3 neuron. The unitary excitatory postsynaptic potentials (EPSPs) sustained for long observation periods, and increased in size with increases in stimulus frequency and in external Ca2+ concentration. This technique may be useful for quantal analysis of transmission through the synapse between mossy fibers and CA3 neurons.

Action Potentials↗
PubMed1989

Variance analysis of excitatory postsynaptic potentials in cat spinal motoneurons during posttetanic potentiation.

1. Fluctuations in the peak amplitudes of composite excitatory postsynaptic potentials (EPSPs) in cat spinal motoneurons were analyzed during posttetanic potentiation (PTP). Each of a series of identical tetanic stimulus trains delivered to a muscle nerve was followed by 45 test stimuli applied at 2-s intervals. The mean peak amplitude and mean peak variance were calculated for EPSPs evoked by all those stimuli following a tetanus with the same time interval. It was assumed that the variance arises primarily from the probabilistic all-or-none behavior of single synaptic boutons and background noise due to spontaneous synaptic activity and thermal noise in the recording system. The variance was corrected for the contribution from additive Gaussian background noise. 2. If it is assumed that individual synaptic boutons behave independently, corrected mean peak variance and mean peak amplitude are related by a parabolic function. The expected parabolic relationship was seen in 9 of 31 cases studied, and the parameters of the best parabolic fit to the data allowed estimation of some synaptic properties. From these parameters, the mean amplitude of the unit EPSP (v) was estimated to be 102.1 +/- 57.4 (SD) microV. An average of 3.7 boutons comprised each Ia-motoneuron contact system. 3. On average, only 27% of all synaptic boutons given off by the stimulated Ia fibers to one motoneuron were active and releasing transmitter during unpotentiated reflex transmission. The remaining 73% of the synapse population was intermittently silent. The population of boutons which took part in synaptic transmission could be divided into two subpopulations, one with a release probability P = 1 and a second with a mean release probability P = 0.13 +/- 0.086. 4. We conclude that synaptic boutons connecting Ia afferents to motoneurons exist in two populations, one having a high and one a low probability of transmitter release. Transmitter release is quantal, resulting in a unit EPSP of approximately 100 microV measured at the motoneuron soma.

Analysis of Variance↗
PubMed1987

Excitatory postsynaptic potentials in neonatal rat sympathetic preganglionic neurons: possible mediation by NMDA receptors.

Excitatory postsynaptic potentials (EPSPs) evoked in antidromically identified sympathetic preganglionic neurons (SPNs) and membrane depolarizations induced by N-methyl-D-aspartate (NMDA) applied by pressure ejection were increased by removing Mg ions from the perfusing media and blocked by D-2-amino-5-phosphonovalerate (APV), DL-APV and ketamine. Further, the amplitude of EPSPs and NMDA-induced depolarizations were decreased and increased by membrane hyperpolarization in Krebs solution with and without Mg2+, respectively. These findings indicate that the excitatory amino acid receptor mediating the EPSPs in SPNs may be of the NMDA subtype.

Animals↗
PubMed1976

Analysis of the slow excitatory postsynaptic potential in bullfrog sympathetic ganglion cells.

The ionic mechanism of the slow excitatory postsynaptic potential (slow EPSP), i.e. the muscarinic action of acetylcholine (ACh), was studied either by stimulating preganglionic nerves or by applying ACh in curarized sympathetic ganglion cells of bullfrogs. There are three different types of cells characterized by the effects of membrane hyperpoliarization on the amplitude of slow EPSP. One group of cells showed an increase in amplitude (type 1 cell) and, in two other groups of cells, it remained unchanged (type 2 cell) or decreased (type 3 cell), when the membrane was hyperpolarized. Under the muscarinic effects of ACh, the slope membrane conductance was increased (type 1 cell), unchanged (type 2 cell) or decreased (type 3 cell) at 10-20 mV hyperpolarized levels, while it was unchanged (type 1 cell) or decreased (types 2 and 3 cells) at resting and depolarized levels. In all cells, the slow ACh potential, corresponding to the slow EPSP, was almost completely suppressed in a high K+, Ca2+-free, Na+-free solution. These results suggest that the slow EPSP is generated by increases in Na+ and Ca2+ conductance and also by a simultaneous decrease in the K+ conductance.

Acetylcholine↗
PubMed1992

Quantal parameters of "minimal" excitatory postsynaptic potentials in guinea pig hippocampal slices: binomial approach.

Binomial distributions of amplitudes of excitatory postsynaptic potentials (EPSPs) mixed with Gaussian noise were simulated. The objective of Monte Carlo simulations was, firstly, to study influences of sampling size (N) and noise standard deviation (Sn) on estimates of mean quantal content (m), quantal size (v) and binomial parameters (n and p) by four methods of quantal analysis (histogram, variance, failures and combined method) based on the binomial model and, secondly, to modify these methods on the basis of comparison of estimated with simulated parameters. Reliable estimates (within +/- 10% of the simulated values) were obtained for large sample sizes (N = 500-1000) with Sn less than or equal to v by the histogram (deconvolution) method and with Sn less than or equal to 2v by the other three methods. Similar results were obtained by averages from about 10 simulations if smaller samples were used (N = 50-200). In electrophysiological experiments on slices, "minimal" EPSPs were recorded from CA1 pyramidal cells after low-intensity stimuli to stratum radiatum or stratum oriens. Amplitudes of minimal EPSPs fluctuated in a manner predicted by the quantum hypothesis. Amplitude distributions of EPSPs in the non-facilitated state were adequately described either by binomial statistics with an average p equal to about 0.4 (a range of 0.3-0.7) and an average n of about 3 (range 2-6) or by Poisson statistics with m of about 1. The quantal analysis suggests that typical values of m and v for a single activated fibre in stratum radiatum might be about 0.5-1 and 300-400 microV, respectively, with low p (0.1-0.3) and n (2-4). However, the estimates of binomial parameters should be considered as coarse approximations in view of the simulation results and a possible nonuniformity of parameter p. The comparison of results of various methods based on the binomial model, in both simulation and physiological experiments, indicates the reliability of estimates of basic quantal parameters (m and v) under realistic conditions of physiological experiments. The methods are considered to be sufficiently sensitive to make use of them for studies on mechanisms of long-term synaptic plasticity.

Animals↗
PubMed1990

Long-lasting facilitation of excitatory postsynaptic potentials in the rat hippocampus by acetylcholine.

1. The effects of acetylcholine (ACh) on excitatory postsynaptic potentials (EPSPs) evoked by stimulating Schaffer-commissural afferents and on ionophoretically applied L-glutamate ligands, were investigated in CA1 neurones of hippocampal slices using current- and voltage-clamp techniques. 2. ACh produced a transient suppression followed by a long-lasting facilitation of EPSPs. The facilitation was also seen in Cs(+)-filled cells under voltage-clamp conditions. Both suppressing and facilitating effects were blocked by atropine. 3. All components of the EPSP were reduced in the initial phase of ACh action, while only the slow component was enhanced during the later phase. The facilitation was blocked by an N-methyl-D-aspartate (NMDA) receptor antagonist, d-2-amino-5-phosphonovalerate (2-APV) and by hyperpolarization. 4. ACh also facilitated responses to ionophoretically applied NMDA in voltage-clamped, Cs(+)-filled cells in Ba2(+)-treated slices. ACh facilitated responses to L-glutamate which was blocked by 2-APV. ACh failed to affect responses to kainate or quisqualate. 5. We conclude that ACh, acting on muscarinic receptors, exerts a primary effect in the hippocampus to specifically amplify NMDA receptor-mediated synaptic responses and thereby facilitate EPSPs.

Acetylcholine↗
PubMed1979

A comparative study of ventrolateral and recurrent excitatory postsynaptic potentials in large pyramidal tract cells in the cat.

In acute cats deeply anesthetized with Nembutal, monosynaptic excitatory postsynaptic potentials (EPSPs) triggered by stimulation of the ventrolateral (VL) thalamic nucleus and the pes pedunculus were recorded in large pyramidal tract cells (PT cells). Deep anesthesia, low intensities of stimulation and an averaging technique were used in order to get VL and recurrent EPSPs free of polysynaptic potentials. Comparison of the time course of both EPSPs revealed a much faster rise time and shorter half-width for VL EPSPs than for recurrent EPSPs. This would suggest a more proximal location for VL synaptic contacts than for recurrent ones with respect to the soma of PT cells. The separation of the sites of origin of both EPSPs is further suggested by their almost perfect linear summation. It is suggested that VL EPSPs are produced on the apical dendritic tree, while recurrent EPSPs could originate on the basilar dendritic branches.

Animals↗
PubMed1992

Miniature excitatory postsynaptic potentials in embryonic motoneurons grown in slice cultures of spinal cord, dorsal root ganglia and skeletal muscle.

Miniature excitatory postsynaptic potentials (mEPSPs) were recorded in motoneurons grown in organotypic cocultures of embryonic rat spinal cord, dorsal root ganglia and muscle in the presence of TTX. The motoneurons were electrically compact with a mean electrotonic length of 0.6. Spontaneous EPSPs were found in most of these motoneurons. With TTX the large EPSPs disappeared, whereas in more than half of the experiments mEPSPs persisted with a range in size of 1 to 4 mV (mean: 2.1 mV), probably originating from the spontaneous release of single vesicles. The net inward charge transfer at the soma ranged from 0.12 to 0.34 pC. The mEPSPs were heterogeneous in size even within pools of potentials that were homogeneous in shape. They had similar shapes and amplitudes as the smallest spontaneous unitary EPSPs mediated by presynaptic impulses, suggesting that for the smallest afferents not more than one vesicle was released per afferent impulse. Both the miniature and the TTX-sensitive EPSPs were readily blocked by the glutamate antagonist DNQX.

Animals↗
PubMed1989

Kynurenic acid antagonizes the excitatory postsynaptic potential elicited in neostriatal neurons in the in vitro slice of the rat.

Stimulation of corpus callosum in rat brain slices evoked an excitatory postsynaptic potential (EPSP) in neostriatal neurons. This EPSP is greatly reduced by exposing the slice to kynurenic acid (KY). The action of KY is reversed when the preparation is bathed in normal Ringer's solution. KY reduces the EPSP amplitude in a dose-dependent fashion, with 1 mM KY attenuating the potential by 86%. The effect is not due to a conductance change, since KY treatment does not alter the neuron's input resistance.

Action Potentials↗