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Results for “Excitatory Postsynaptic Potentials”

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At least 19 recordsLinked to original sources

PubMed1984

Differential and selective antagonism of the slow-inhibitory postsynaptic potential and slow-excitatory postsynaptic potential by gallamine and pirenzepine in the superior cervical ganglion of the rabbit.

Two cholinergic antagonists, gallamine and pirenzepine, agents that have been shown to bind selectively to different subpopulations of the muscarinic receptor, were found to antagonize selectively and differentially the amplitudes of the slow-inhibitory and slow-excitatory postsynaptic potentials in the superior cervical ganglion of the rabbit. Incubation of ganglia with gallamine resulted in a concentration-dependent suppression of the slow-inhibitory postsynaptic potential. The pharmacological action of gallamine was highly specific. At concentrations which reduced the amplitude of the slow-inhibitory postsynaptic potential by as much as 70-90%, there was no reduction of the amplitudes of the muscarinic slow-excitatory postsynaptic potential, the nicotinic fast-excitatory postsynaptic potential, noncholinergic slow-slow-excitatory postsynaptic potential, or post-stimulus hyperpolarizing afterpotentials. The amplitude of the slow-excitatory postsynaptic potential was actually facilitated in the presence of gallamine, presumably as a result of suppression of the overlapping slow-inhibitory postsynaptic potential. In contrast to the action of gallamine, pirenzepine produced a selective suppression of the amplitude of the slow-excitatory postsynaptic potential. Pirenzepine had very little influence on the amplitude of the slow-inhibitory postsynaptic potential at concentrations sufficient to reduce the amplitude of the slow-excitatory postsynaptic potential by as much as 50%, and had no effect on the amplitudes of the nicotinic fast-excitatory postsynaptic potential or noncholinergic slow-slow-excitatory postsynaptic potential. The evidence presented suggests that multiple muscarinic recognition sites, previously identified by studies of the affinities of pharmacological agents for the muscarinic receptor, may actually be involved in synaptic transmission and functionally coupled to cellular effector mechanisms.

Animals↗

PubMed2006

17beta-Estradiol potentiates field excitatory postsynaptic potentials within each subfield of the hippocampus with greatest potentiation of the associational/commissural afferents of CA3.

We sought to determine the impact of 17beta-estradiol throughout the hippocampal trisynaptic pathway and to investigate the afferent fiber systems within CA1 and CA3 in detail. To achieve this objective, we utilized multielectrode arrays to simultaneously record the field excitatory postsynaptic potentials from the CA1, dentate gyrus, and CA3 of rat hippocampal slices in the presence or absence of 100 pM 17beta-estradiol. We confirmed our earlier findings in CA1, where 17beta-estradiol significantly increased field excitatory postsynaptic potentials amplitude (20%+/-3%) and slope (22%+/-7%). 17beta-Estradiol significantly potentiated the field excitatory postsynaptic potentials in dentate gyrus, amplitude (15%+/-4%) and slope (17%+/-5), and in CA3, amplitude (15%+/-4%) and slope (19%+/-5%). Using a high-density multielectrode array, we sought to determine the source of potentiation in CA1 and CA3 by determining the impact of 17beta-estradiol on the apical afferents and the basal afferents within CA1 and on the mossy fibers and the associational/commissural fibers within CA3. In CA1, 17beta-estradiol induced a modest increase in the amplitude (7%+/-2%) and slope (9%+/-3%) following apical stimulation with similar magnitude of increase following basal stimulation amplitude (10%+/-2%) and slope (12%+/-3%). In CA3, 17beta-estradiol augmented the mossy fiber amplitude (15%+/-3%) and slope (18%+/-6%) and the associational/commissural fiber amplitude (31%+/-13%) and slope (40%+/-15%). These results indicate that 17beta-estradiol potentiated synaptic transmission in each subfield of the hippocampal slice, with the greatest magnitude of potentiation at the associational/commissural fibers in CA3. 17beta-Estradiol regulation of CA3 responses provides a novel site of 17beta-estradiol action that corresponds to the density of estrogen receptors within the hippocampus. The implications of 17beta-estradiol potentiation of the field potential in each of the hippocampal subfields and in particular CA3 associational/commissural fibers for memory function and clinical assessment are discussed.

Afferent Pathways↗

PubMed1998

Principal component analysis of minimal excitatory postsynaptic potentials.

'Minimal' excitatory postsynaptic potentials (EPSPs) are often recorded from central neurones, specifically for quantal analysis. However the EPSPs may emerge from activation of several fibres or transmission sites so that formal quantal analysis may give false results. Here we extended application of the principal component analysis (PCA) to minimal EPSPs. We tested a PCA algorithm and a new graphical 'alignment' procedure against both simulated data and hippocampal EPSPs. Minimal EPSPs were recorded before and up to 3.5 h following induction of long-term potentiation (LTP) in CA1 neurones. In 29 out of 45 EPSPs, two (N=22) or three (N=7) components were detected which differed in latencies, rise time (Trise) or both. The detected differences ranged from 0.6 to 7.8 ms for the latency and from 1.6-9 ms for Trise. Different components behaved differently following LTP induction. Cases were found when one component was potentiated immediately after tetanus whereas the other with a delay of 15-60 min. The immediately potentiated component could decline in 1-2 h so that the two components contributed differently into early (< 1 h) LTP1 and later (1-4 h) LTP2 phases. The noise deconvolution techniques was applied to both conventional EPSP amplitudes and scores of separate components. Cases are illustrated when quantal size (upsilon) estimated from the EPSP amplitudes increased whereas upsilon estimated from the component scores was stable during LTP1. Analysis of component scores could show apparent double-fold increases in upsilon which are interpreted as reflections of synchronized quantal releases. In general, the results demonstrate PCA applicability to separate EPSPs into different components and its usefulness for precise analysis of synaptic transmission.

Algorithms↗

PubMed1983

Synaptic interactions between mammalian central neurons in cell culture. I. Reversal potential for excitatory postsynaptic potentials.

Intracellular recording and stimulation techniques were used to study the electrical properties of neurons in cell cultures from fetal mouse spinal cord (SC). The morphology of SC neurons and the distribution on SC neurons of boutons formed by synaptically connected SC or dorsal root ganglion (DRG) neurons were demonstrated with horseradish peroxidase (HRP) injection. Postsynaptic polarization in conjunction with synaptic activation of SC neurons was used to determine the reversal potential for excitatory postsynaptic potentials (EPSPs). Tetraethylammonium ions were injected postsynaptically in order to obtain reversal of the EPSPs. Both SC-SC and DRG-SC excitatory connections could be reversed by postsynaptic depolarization. The average reversal potential for the SC-SC EPSP was -4 +/- 12.2 (SD) mV and that for the DRG-SC EPSP was +8 +/- 7.9 (SD) mV, a statistically significant difference (Wilcoxon two-sample rank; P less than 0.05). Scatter was quite large, particularly for the SC-SC connection. While some neurons gave clear electrophysiological evidence of significant dendritic effects, the average total electrotonic length was small (0.58 +/- 0.65 (SD) of a length constant). The morphological extent of the dendrites of SC neurons was substantially less than that of mature motoneurons in vivo. We concluded that both SC-SC and DRG-SC EPSPs were mediated by a conventional conductance increase and that most synaptic input was not far removed electrically from the recording site in the neuron cell body.

Animals↗

PubMed1980

Potentiation of excitatory postsynaptic potentials during and after repetitive stimulation in thin hippocampal sections.

Excitatory postsynaptic potentials (EPSPs) elicited by mossy fiber stimulation were recorded intracellularly from neurons in the CA3 region in thin hippocampal sections in vitro and potentiation of the EPSPs was examined during and after repetitive stimulation. Inhibitory postsynaptic potentials (IPSPs) and seizure discharges were blocked by bicuculline and high concentrations of Mg2+. When two shocks were applied at short intervals, the second EPSP was markedly potentiated. This potentiation declined exponentially with a time-constant of about 180 ms and was unaffected by changes in ambient temperature. The amount of potentiation during a pulse train was explained by summation of potentiation by individual pulses. Post tetanic potentiation lasted longer in media containing Ca2+ at higher concentrations and Mg2+ at lower concentrations. At high Ca2+ concentrations, tetanic stimulation induced long-term potentiation which was occasionally preceded by a long-lasting suppression. Tetanus to a bundle of mossy fibers potentiated EPSPs elicited by stimulation of a separate bundle of mossy fibers (heterosynaptic potentiation) but did not augment EPSPs elicited by fimbrial stimulation.

Animals↗

PubMed1995

Thalamocortical and corticocortical excitatory postsynaptic potentials mediated by excitatory amino acid receptors in the cat motor cortex in vivo.

Intracellular recordings were made from neurons in the motor cortex of an anaesthetized cat, together with iontophoretic application of excitatory amino acid receptor agonists and antagonists, in order to evaluate the role of such receptors in excitatory postsynaptic potentials evoked from stimulation of afferent and recurrent pathways in vivo. Excitatory postsynaptic potentials which were evoked by stimulation of the ventrolateral thalamus were found to be largely insensitive to antagonism by N-methyl-D-aspartate receptor antagonists, although they were susceptible to blockade by the non-N-methyl-D-aspartate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione. Increasing the ventrolateral thalamus stimulation frequency from 0.5 or 1 to 5 Hz caused an increase of evoked excitatory postsynaptic potential amplitudes and number of action potentials. These augmented excitatory postsynaptic potentials remained insensitive to application of N-methyl-D-aspartate antagonists. In contrast, recurrent excitatory postsynaptic potentials evoked by stimulation of the pyramidal tract were found to be sensitive to N-methyl-D-aspartate receptor antagonists and/or non-N-methyl-D-aspartate receptor antagonists in some neurons. These results demonstrate the involvement of both N-methyl-D-aspartate- and non-N-methyl-D-aspartate receptors in synaptic responses of cat motor cortex neurons in vivo, and that the synaptic pharmacology of the thalamic input may differ from that of the local recurrent pathways.

2-Amino-5-phosphonovalerate↗

PubMed1995

Potentiation of excitatory postsynaptic potentials by a metabotropic glutamate receptor agonist (1S,3R-ACPD) in frog spinal motoneurons.

We conducted intracellular recordings of lumbar motoneurons in the arterially-perfused frog spinal cord and investigated the effects of a metabotropic glutamate receptor agonist, (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD), on excitatory postsynaptic potentials evoked by stimulation of the descending lateral column fibers (LC-EPSPs). In the absence of Mg2+, ACPD reversibly potentiated the amplitude of monosynaptic LC-EPSPs by more than 15% in 15 of 19 cells with 5 microM ACPD and in 7 of 12 cells with 0.5 microM ACPD. The EPSP amplitudes with 5 and 0.5 microM ACPD were 142 +/- 10% (mean +/- S.E.M., n = 19) and 130 +/- 13% (n = 12) of the controls. The potentiation was seen without a decrease in the input conductance. Glutamate-induced depolarizations in the absence and the presence of 0.5 microM ACPD were not significantly different in cells perfused with the low Ca(2+)-high Mg2+ solution which eliminated chemical transmission. Paired pulse facilitation of LC-EPSPs was reversibly decreased in association with the potentiation. ACPD-induced potentiation of monosynaptic LC-EPSPs was seen in 5 of 6 cells in the presence of D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5), an NMDA receptor antagonist. ACPD occasionally activated polysynaptic components of LC-EPSPs which were mediated mainly via NMDA receptors. On the other hand, ACPD-induced potentiation of EPSPs was inhibited by extracellular Mg2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Differential effects of pentylenetetrazol-kindling on long-term potentiation of population excitatory postsynaptic potentials and population spikes in the CA1 region of rat hippocampus.

The effects of pentylenetetrazol-kindling on synaptic transmission and the effectiveness of θ pattern primed-bursts (PBs) for the induction of long-term potentiation (LTP) of population excitatory postsynaptic potentials and population spikes were investigated in hippocampal CA1 of pentylenetetrazol-kindled rats. Experiments were carried out in the control and kindled animals at two post-kindling periods, i.e., 48-144 h (early phase) and 30-33 days (long lasting phase). Field potentials (population excitatory postsynaptic potentials, pEPSPs; and population spikes, PSs) were recorded at the stratum radiatum and the stratum pyramidale following stimulation of the stratum fibers, respectively. PBs were delivered to stratum fibers and PB potentiation was assessed. The results showed that 48-144 h after kindling there was no significant difference for pEPSP slope and PS amplitude between two groups. But at 30-33 days after kindling, the pEPSP slope in the stratum radiatum of kindled animals decreased, whereas the amplitude of PSs increased compared to those of controls. Shortly after kindling, control animals had normal LTP of pEPSP slope and PS amplitude in response to PBs, but kindled rats lack LTP of pEPSP slope and PBs induced LTP of PS amplitude in most of kindled animals. In 30-33 days after kindling, PB potentiation was not observed in the stratum radiatum of kindled animals but PBs induced LTP of PS amplitude, which was significantly greater than that of control animals. The effect is compatible with the hypothesis, which postulates kindling-associated functional deficit in hippocampus, especially CA1, as an explanation for the behavioral deficits seen with the kindling model of epilepsy.

Action Potentials↗

PubMed1998

Calcium dynamics in single spines during coincident pre- and postsynaptic activity depend on relative timing of back-propagating action potentials and subthreshold excitatory postsynaptic potentials.

We compared the transient increase of Ca2+ in single spines on basal dendrites of rat neocortical layer 5 pyramidal neurons evoked by subthreshold excitatory postsynaptic potentials (EPSPs) and back-propagating action potentials (APs) by using calcium fluorescence imaging. AP-evoked Ca2+ transients were detected in both the spines and in the adjacent dendritic shaft, whereas Ca2+ transients evoked by single EPSPs were largely restricted to a single active spine head. Calcium transients elicited in the active spines by a single AP or EPSP, in spines up to 80 micro(m) for the soma, were of comparable amplitude. The Ca2+ transient in an active spine evoked by pairing an EPSP and a back-propagating AP separated by a time interval of 50 ms was larger if the AP followed the EPSP than if it preceded it. This difference reflected supra- and sublinear summation of Ca2+ transients, respectively. A comparable dependence of spinous Ca2+ transients on relative timing was observed also when short bursts of APs and EPSPs were paired. These results indicate that the amplitude of the spinous Ca2+ transients during coincident pre- and postsynaptic activity depended critically on the relative order of subthreshold EPSPs and back-propagating APs. Thus, in neocortical neurons the amplitude of spinous Ca2+ transients could encode small time differences between pre- and postsynaptic activity.

Action Potentials↗

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↗

PubMed2002

Bidirectional plasticity of excitatory postsynaptic potential (EPSP)-spike coupling in CA1 hippocampal pyramidal neurons.

Integration of synaptic excitation to generate an action potential (excitatory postsynaptic potential-spike coupling or E-S coupling) determines the neuronal output. Bidirectional synaptic plasticity is well established in the hippocampus, but whether active synaptic integration can display potentiation and depression remains unclear. We show here that synaptic depression is associated with an N-methyl-d-aspartate receptor-dependent and long-lasting depression of E-S coupling. E-S depression is input-specific and is expressed in the presence of gamma-aminobutyric acid type A and B receptor antagonists. In single neurons, E-S depression is observed without modification of postsynaptic passive properties. We conclude that a decrease in intrinsic excitability underlies E-S depression and is synergic with glutamatergic long-term depression.

Animals↗

PubMed1995

Simultaneous expression of excitatory postsynaptic potential/spike potentiation and excitatory postsynaptic potential/spike depression in the hippocampus.

Tetanic stimulation of afferents in the stratum radiatum of the CA1 area of the rat hippocampus results in long-term potentiation of excitatory synaptic responses in pyramidal cells. Previous studies have reported a greater increase in the population spike amplitude following the induction of long-term potentiation than could be accounted for by the increase of the slope of the population excitatory postsynaptic potential. Two hypotheses have been proposed to explain this phenomenon (called excitatory postsynaptic potential/spike potentiation): a modification of the firing threshold and/or a modification of the inhibitory drive. Previous studies have not, however, addressed the question of possible changes in spike threshold in association with long-term depression. This paper examines whether the concomitant long-term potentiation of pharmacologically isolated N-methyl-D-aspartate receptor-mediated excitatory postsynaptic potentials, reported previously, is also associated with a change in spike threshold. When the amplitude of the population spike is plotted as a function of the slope of the population excitatory postsynaptic potential (excitatory postsynaptic potential/spike curve), excitatory postsynaptic potential/spike potentiation (depression) is seen as a shift of the excitatory postsynaptic potential/spike curve to the left (right) following a conditioning stimulus. In this study, using kainic acid lesioned hippocampus, we have shown that tetanic stimulation produced excitatory postsynaptic potential/spike potentiation of the control synaptic response and excitatory postsynaptic potential/spike depression of the isolated N-methyl-D-aspartate receptor-mediated responses.

2-Amino-5-phosphonovalerate↗

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↗

PubMed1998

Interaction between paired-pulse facilitation and long-term potentiation of minimal excitatory postsynaptic potentials in rat hippocampal slices: a patch-clamp study.

Long-term potentiation is an experimental paradigm used to study synaptic plasticity and memory mechanisms. One similarity between long-term potentiation and memory is the existence of several distinct phases. However, our preliminary quantal analysis did not reveal essential differences in expression mechanisms of the early (< 1 h) and later (up to 3 h) phases of long-term potentiation. The data were compatible with presynaptic mechanisms of both phases. Another approach to distinguish between presynaptic and postsynaptic mechanisms is analysis of interaction between long-term potentiation and presynaptic paired-pulse facilitation. Such analysis had been previously done mainly with recordings of field potentials reflecting the activity of large neuronal populations. Only the early potentiation phase had been previously analysed with recordings from single neurons. The results from different groups were contradictory. In the present study, minimal excitatory postsynaptic potentials were recorded from CA1 pyramidal neurons of rat hippocampal slices. Paired-pulse facilitation ratios were calculated for various periods (up to 2-3 h) following induction of long-term potentiation. The ratio persistently decreased in the majority of neurons following long-term potentiation induction. The decrease in the paired-pulse facilitation ratio correlated with the magnitude of long-term potentiation and with the initial (pretetanic) facilitation ratio. Therefore, the general results of the present analysis was similar with the results of the quantal analysis: it is consistent with a strong involvement of presynaptic mechanisms in maintenance of both early and late phases of long-term potentiation. However, individual neurons could show variable changes in the paired-pulse facilitation, e.g., increases at late (> 0.5-1 h) periods after tetanus. Calculations of partial correlations and regression analysis indicated that positive correlation between potentiation magnitude and initial (pretetanic) paired-pulse facilitation tended to increase in the late potentiation phase (1.5-2.5 h post-tetanus) indicating that different mechanisms are involved in the early (0.5 h post-tetanus) and the late phase of long-term potentiation. The findings are compatible with involvement of presynaptic mechanisms in both the early and late phases of long-term potentiation. However, the results suggest that contribution of changes in release probability and in effective number of transmitter release sites may differ during the two phases. It is suggested that activation of silent synapses and increases in the number of transmission zones due to pre- and postsynaptic structural rearrangements represent important mechanisms of the late phase of long-term potentiation.

Animals↗

PubMed1995

The complementary nature of long-term depression and potentiation revealed by dual component excitatory postsynaptic potentials in hippocampal slices from young rats.

Homosynaptic long-term depression and long-term potentiation were studied in hippocampal slices from 12-18-day-old rats using field excitatory postsynaptic potentials recorded in the CA1 subfield (stratum radiatum). Independent estimates of the alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) and the N-methyl-D-aspartate receptor-mediated components of the field excitatory postsynaptic potential were obtained in parallel using early and late measurements of a dual component excitatory postsynaptic potential in a solution containing low (0.1 mM) magnesium and 1 microM of the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Long-term depression, induced by 2 Hz stimulation for 10 min, was observed as an equal relative depression of the AMPA and N-methyl-D-aspartate receptor-mediated components of the field excitatory postsynaptic potential, whereas long-term potentiation induced by single or repeated high-frequency stimulation, was seen initially as a predominant potentiation of the AMPA receptor-mediated component. Within the first 30-60 min, long-term potentiation gradually changed to more equal increases of the two components of the excitatory postsynaptic potential. During alternating induction of long-term depression and long-term potentiation, the AMPA and N-methyl-D-aspartate receptor-mediated components could both be repeatedly regulated up and down. Long-term depression and long-term potentiation also showed several signs of interaction with each other during such experiments; e.g., long-term depression removed the occlusive effect of large long-term potentiation on a subsequent long-term potentiation, and long-term potentiation applied after the induction of long-term depression was found to be more stable than otherwise. The results support the notion that long-term depression and long-term potentiation employ changes in a common synaptic property. A tentative mechanism for this modification, expressed as equal changes of AMPA and N-methyl-D-aspartate receptor-mediated components of the excitatory postsynaptic potential, is an alteration in transmitter release, while the initial asymmetric part of long-term potentiation indicates involvement of an additional short-term modification.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

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↗

PubMed1994

Influence of temperature on anoxic responses of neocortical pyramidal neurons.

Intracellular recordings were made in pyramidal neurons of layers II-III of rat fronto-parietal neocortical slices. The membrane and synaptic properties and effects of brief (4-6 min) anoxia-anoxic depolarization and synaptic depression--were recorded at temperatures between 26 and 37.5 degrees C. In normoxic conditions, both warming (> or = 35 degrees C) and cooling (< or = 32 degrees C) induced a reduction in the amplitude of early and late excitatory postsynaptic potentials and abolished inhibitory postsynaptic potentials. Excitatory postsynaptic potential latency decreased with warming and increased with cooling. Warming also induced spontaneous brief depolarizations, had a general slow depolarizing effect on resting membrane potential, and decreased input resistance. During oxygen deprivation, the steepness of the rising phase of the anoxic depolarization and the duration of the repolarization phase were augmented by warming above 36.5 degrees C (3.7 +/- 0.1 vs 1.9 +/- 0.1 mV/min and 8.75 +/- 0.98 vs 4.16 +/- 0.28 min, respectively). The peak amplitude of the anoxic depolarization increased in only one-third of trials (6.6 +/- 0.6 vs 4.3 +/- 0.4 mV). Warming potentiated the depressant effect of anoxia: at 36.5 degrees C early excitatory postsynaptic potential amplitude decreased to 32.3 +/- 5.2% of control compared with 58.3 +/- 1.2% at 33.5 degrees C, the late excitatory postsynaptic potential was abolished in < 2 min, and the recovery of the compound excitatory postsynaptic potential was prolonged (12.8 +/- 0.8 vs 7.8 +/- 0.3 min). Cooling reduced the amplitude of the anoxic depolarization and increased the input resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗