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At least 127 records · Page 7Linked to original sources
PubMed1992

Analysis of fluctuations of "minimal" excitatory postsynaptic potentials during long-term potentiation in guinea pig hippocampal slices.

In previous studies, quantal analysis assuming a simple binomial model has shown that long-term potentiation (LTP) is accompanied by an increase in both mean quantal content (m) and quantal size (v), whereby the increase in m predominates. In the present study, "compound" binomial distributions with variable probabilities were convolved with Gaussian distributions in computer experiments to simulate amplitude histograms of intracellular excitatory postsynaptic potentials (EPSPs). A deconvolution procedure assuming equal "quantal" separation (v) between discrete components, but without assuming binomial statistics, was applied to the simulated distributions to determine v. It was found that with a small ratio of standard deviation of noise to v (Sn/v less than 0.4), a reliable estimate of v can be obtained even for small samples (N = 100). When Sn/v was larger (0.4-0.6), approximate v estimates (within +/- 10-20% of the simulated v) could be obtained by averaging estimates from about 10 small samples (N = 100). "Minimal" EPSPs were recorded in area CA1 of guinea pig hippocampal slices. 37 EPSP amplitude samples of 9 neurones were measured before and up to 55 min after 10 tetanizations of stratum radiatum. In accordance with the previous data, the increase in v accounted for only about 10% of the average post-tetanic increase in EPSP amplitude and was not correlated with the latter. However, for an EPSP subset with small LTP magnitude, the increase in v accounted for an essential part of the LTP magnitude while the increase in m did not correlate with it. The results are in agreement with previous data obtained in the context of the simple binomial model and are interpreted as indicating primarily a presynaptic mechanism of LTP maintenance. The results suggest two types of synaptic mechanism of LTP maintenance related to the increases in m and v, respectively. The latter mechanism is saturated at about 10 to 30% increase in post-tetanic amplitude above the pre-tetanic EPSP amplitude.

Animals↗
PubMed1991

Excitatory postsynaptic potentials evoked by ventral root stimulation in neonate rat motoneurons in vitro.

1. Intracellular recordings were made from antidromically identified motoneurons in transverse (500 microns) lumbar spinal cord slices of neonatal (12-20 day) rats. 2. Electrical stimulation of ventral rootlets evoked, with or without an antidromic spike or initial segment potential, a depolarizing response (latency, 1-4.2 ms), a hyperpolarizing response (latency, 1.5-3.5 ms), or a combination of two preceding responses in 38, 6, and 8% of motoneurons investigated. 3. The hyperpolarizing response was reversibly eliminated by low Ca2+ (0.25 mM), d-tubocurarine (d-Tc; 10 microM) or strychnine (1 microM), suggesting that this response represents an inhibitory post-synaptic potential (IPSP) mediated by glycine or a related substance release from inhibitory interneurons subsequent to their activation by axon collaterals in a manner analogous to the Renshaw cell circuitry described for the cat motoneurons. 4. The depolarizing responses were excitatory postsynaptic potentials (EPSPs), because they could be graded by varying the stimulus intensity and were reversibly abolished in low Ca2+ solution. 5. Membrane hyperpolarization increased the amplitude of EPSPs, and the mean extrapolated reversal potential was -4 mV. 6. EPSPs were augmented, rather than diminished, by dihydro-beta-erythroidine (1 microM) or d-Tc, arguing against a role of recurrent motor axon collaterals in initiating the responses. 7. The conduction velocity of the fibers initiating the EPSPs ranged from 0.35 to 0.96 m/s, indicating that these fibers were unmyelinated. Furthermore, the EPSP exhibited a constant delay when the stimulus frequency was varied from 1 to 5 Hz, and the synaptic delay estimated by extrapolation was less than 1 ms, suggesting that it was a monosynaptic event. 8. After complete separation of the ventral and dorsal horns by a knife cut, stimulation of ventral rootlets could still evoke an EPSP in motoneurons. 9. Superfusion of the slices with the nonselective glutamate receptor antagonist kynurenic acid (0.2-1 mM) or the selective quisqualate/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) (0.5-1 microM) reversibly diminished the EPSPs. 10. EPSPs evoked by stimulation of dorsal and ventral rootlets exhibited different latency and waveform in the same motoneurons. 11. The results provide evidence that activation of ventral root afferents evoked an EPSP mediated by glutamate or a related substance in a population of motoneurons. Furthermore, the afferent pathway mediating the EPSP appears to be monosynaptic and confined to the ventral horn.

Action Potentials↗
PubMed1991

Composition of the excitatory postsynaptic potentials recorded from rat visual cortical neurons in layer. II/III: An in vitro electrophysiological and pharmacological studies.

Intracellular recordings were performed on layer II/III neurons of rat brain slices. Neuronal responses to electrical stimulation of the white matter was analyzed pharmacologically using D-2-amino-5-phosphonovalerate (APV), a specific antagonist of the N-methyl-D-aspartate (NMDA) receptor, and kynurenate (Kyn), a broad-spectrum antagonist of both the NMDA and the non-NMDA (kainate and quisqualate) receptors. Fifty-five neurons produced an excitatory postsynaptic potential (EPSP) in response to a single shock. In forty-eight neurons (87%) of them, the EPSP consisted of an APV-sensitive component and an APV-insensitive component. While in seven neurons (13%), it consisted of only the APV-insensitive component. The APV-sensitive component was preceded by the APV-insensitive component and was enhanced in amplitude and duration by the following procedures: a) applying repetitive stimulations to the white matter, b) reducing Mg2+ concentration in the bathing solution and c) depolarizing cell membrane. The APV-insensitive component was affected by neither repetitive stimulation nor reduction of Mg2+ concentration. Both APV-sensitive and APV-insensitive components were reduced by the treatment of Kyn. These suggest that in bathing medium containing Mg2+, the APV-sensitive (i.e. the NMDA receptor-mediated) EPSP is generated by the non-NMDA receptor-mediated depolarization, which removes the Mg2+ blockade in NMDA receptor-gated channel.

2-Amino-5-phosphonovalerate↗
PubMed1985

Pharmacology of the corticocaudate excitatory postsynaptic potential in the cat: evidence for its mediation by quisqualate- or kainate-receptors.

Caudate neurons were recorded with intracellular electrodes in halothane anaesthetized cats during microiontophoretic application of drugs and simultaneous stimulation of the corticocaudate pathway. Application of 2-amino-7-phosphonoheptanoic acid inhibited excitations induced by the N-methyl-D-aspartic acid receptor agonists N-methyl-D-aspartic acid and quinolinic acid, but not those elicited by quisqualic acid or activation of the cortico-caudate pathway. Selective inhibition of N-methyl-D-aspartic acid induced excitations was also found in vitro in the frog hemisected spinal cord preparation where a pA2-value of 5.5 against N-methyl-D-aspartic acid was determined. The endogenous tryptophan metabolite, kynurenic acid, antagonized excitations induced by N-methyl-D-aspartic, quisqualic, L-glutamic and kainic acid as well as the excitatory postsynaptic potential (EPSP) evoked in caudate cells by stimulation of the corticocaudate pathway, while action potentials elicited by an intracellularly applied depolarizing current were only slightly affected. In vitro experiments with the frog hemisected spinal cord preparation suggested that kynurenic acid might be a competitive antagonist of both N-methyl-D-aspartate and quisqualate receptors, with pA2-values of about 4.8 and 4.0, respectively. From these results it is concluded that the three-receptor concept for excitatory amino acids are proposed by Watkins and colleagues is probably applicable to the cat caudate nucleus and that the cortically evoked monosynaptic EPSP is mediated by a non-N-methyl-D-aspartate quisqualate- or kainate-receptor.

2-Amino-5-phosphonovalerate↗
PubMed1991

Substance P-mediated slow excitatory postsynaptic potential elicited in dorsal horn neurons in vivo by noxious stimulation.

The original proposal that substance P is involved in the regulation of nociceptive information at the first sensory synapse in the spinal cord has been substantiated by a wide range of evidence, but definitive support has been lacking, due primarily to the lack of evidence that a specific nociceptive response in the dorsal horn can be blocked by a substance P antagonist. Here, we present evidence that CP-96,345, a specific substance P (NK-1) receptor antagonist, selectively blocks a slow, prolonged excitatory postsynaptic potential following noxious cutaneous stimulation or a train of intense electrical stimuli to sensory nerves but does not affect the response to innocuous input or the brief response to single electrical stimuli to C fibers. These results indicate the specific involvement of substance P in the mediation of a prolonged after-excitation to noxious stimulation. This may have important implications for the etiology and treatment of chronic pain and for plastic changes in nociceptive pathways.

Animals↗
PubMed1996

Pairing-specific long-term depression of Purkinje cell excitatory postsynaptic potentials results from a classical conditioning procedure in the rabbit cerebellar slice.

1. Using a rabbit cerebellar slice preparation, we stimulated a classical conditioning procedure by stimulating parallel fiber inputs to Purkinje cells with the use of a brief, high-frequency train of eight constant-current pulses 80 ms before climbing fiber inputs to the same Purkinje cell were stimulated with the use of a brief, lower frequency train of three constant-current pulses. In all experiments, we assessed the effects of stimulation by measuring the peak amplitude of Purkinje cell excitatory postsynaptic potentials (EPSPs) to single parallel fiber test pulses. 2. Intradendritically recorded Purkinje cell EPSPs underwent a long-term (> 20 min) reduction in peak amplitude (30%) after paired stimulation of the parallel and climbing fibers but not after unpaired or parallel fiber alone stimulation. We call this phenomenon pairing-specific long-term depression (PSD). 3. Facilitation of the peak amplitude of a second EPSP elicited by a parallel fiber train occurred both before and after paired stimulation suggesting that the locus of depression was not presynaptic. Depression of the peak amplitude of a depolarizing response to focal application of glutamate following pairings of parallel and climbing fiber stimulation added support to a suggested postsynaptic locus of the PSD effect. 4. The application of aniracetam potentiated EPSP peak amplitude by 40%, but these values returned to baseline as a result of pairings. With the removal of aniracetam from the bath 20 min after pairings, normal levels of pairing-specific EPSP depression were observed, indicating that the effect did not result from direct desensitization of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-proprionic acid (AMPA) receptors. 5. Incubation of slices in the protein kinase inhibitor H-7 potentiated EPSP peak amplitudes slightly (9%), but peak amplitudes returned to baseline levels after pairings. The net reduction in EPSP peak amplitude of < 10% after pairings suggested that H-7 partially blocked PSD and that, in turn, PSD involved protein kinases. 6. The means of induction and the specificity of those means suggest that the phenomenology of PSD is fundamentally different from that of long-term depression. PSD only occurs with pairings of trains of parallel fiber and climbing fiber stimulation; it occurs without the need for bicuculline; and it can overcome the blocking effects of aniracetam. 7. Nevertheless, the involvement of protein kinases and the potential role of calcium suggest that the mechanisms involved in the induction of PSD and long-term depression have a number of features in common. 8. Because of the pairing-specific nature of the long-term synaptic depression observed in these experiments, PSD provides a mechanism that may contribute to the role of the cerebellar cortex in classical conditioning.

Animals↗
PubMed1994

Thyrotropin-releasing hormone enhances excitatory postsynaptic potentials in neocortical neurons of the rat in vitro.

Several lines of evidence suggest a modulatory effect of thyrotropin-releasing hormone (TRH) on synaptic transmission in the mammalian neocortex. In the present study, the effects of this tripeptide on intracellularly recorded neocortical pyramidal neurons were investigated using rat in vitro brain slice preparations. TRH (5 microM and 50 microM) added to the perfusion medium concentration-dependently increased the excitability of pyramidal neurons, reflected by the number of spikes evoked by a depolarizing current pulse and by the augmentation of the time integral of glutamatergic excitatory postsynaptic potentials (EPSPs). TRH increased preferentially the time integrals of the late components of EPSPs (1-EPSPs) and increased their voltage-dependence. The early components of the EPSPs (e-EPSPs) were changed to much lesser extent. Iontophoretically applied D-2-amino-5-phosphonovalerate (D-APV) antagonized the TRH-induced increase of the 1-EPSPs. TRH also markedly enhanced the depolarizing responses evoked by iontophoretically applied N-methyl-D-aspartate (NMDA), while the depolarizing responses evoked by (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and L-glutamate were not significantly affected. The depolarizing inward rectification present in all neurons studied was augmented by the higher concentration of TRH. The effects of TRH were incited after about 5 min and were long-lasting. In most neurons the effects of TRH on neuronal excitability did not completely recover during the 45 min washout period. The present data suggest that some of the non-hormonal actions of TRH in the neocortex may be due to an enhancement of glutamatergic synaptic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1998

[Rapid effect of glucocorticoid on excitatory postsynaptic potential of B cells in bullfrog paravertebral ganglia].

In the present study, the rapid effect of hydrocortisone 21-hemisuccinate (F-suc) on the amplitude of f-EPSP of B cells in isolated bullfrog sympathetic ganglia was examined with the use of intracellular recording technique. It was found that the amplitude of f-EPSP of B cells was decreased by F-suc, with a latency less than 3 min after the beginning of perfusion of F-suc. The inhibition of F-suc was concentration-dependent and could be blocked by the antagonist of intracellular glucocorticoid receptor RU38486, but not by the protein synthesis inhibitor actidione. These findings suggest that the inhibition of f-EPSP of B cells by F-suc is probably mediated through a nongenomic mechanism.

Animals↗
PubMed2004

Enhancement of excitatory postsynaptic potentials by preceding application of acetylcholine in mesencephalic dopamine neurons.

Previously, we reported that Ca(2+) influx through nicotinic acetylcholine (ACh) receptors (nAChRs) activates a fulfenamic acid (FFA)-sensitive inward current, presumably a Ca(2+)-activated nonselective cation current (I(CAN)), in mesencephalic dopamine (DA) neurons. This current exhibited a negative slope conductance in the voltage range between -80 and -40mV and its activation led to a dramatic change in the responses to a transient application of glutamate, from single spikes to burst discharges. In this study, to examine the effect of activation of the FFA-sensitive current on EPSPs, we applied ACh (1mM) by transient air pressure shortly before electrical stimulation to evoke EPSPs in DA neurons. Application of ACh enhanced the amplitude of EPSPs when it preceded the electrical stimulation by less than 2 s, but not when the interval was longer than 3 s. In addition, this enhancement was critically dependent on intracellular Ca(2+) and the membrane potentials of the postsynaptic cell. Furthermore, the enhancing effect of ACh on EPSPs was sensitive to FFA and phenytoin. These results suggest that Ca(2+) influx caused by cholinergic inputs enhances EPSPs via activation of the FFA- and phenytoin-sensitive current.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1991

5-Hydroxytryptamine depresses reticulospinal excitatory postsynaptic potentials in motoneurons of the lamprey.

Application of 5-hydroxytryptamine (5-HT) to the lamprey spinal cord in vitro reversibly depressed the chemical component of excitatory post-synaptic potentials recorded intracellularly in motoneurons and evoked by stimulation of single reticulospinal Müller cells. The depression could be produced either by local application of small volumes of 10 mM 5-HT to the surface of the spinal cord or by bath-application of 1 or 10 microM 5-HT. No effect on the input resistance of the postsynaptic cells or their sensitivity to glutamate, the suspected transmitter at this synapse, could be detected, suggesting the possibility of a presynaptic action of 5-HT at this synapse in the lamprey.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

Serotonin induces excitatory postsynaptic potentials in apical dendrites of neocortical pyramidal cells.

By intracellular and whole cell recording in rat brain slices, it was found that bath-applied serotonin (5-HT) produces an increase in the frequency and amplitude of spontaneous excitatory postsynaptic potentials/currents (EPSPs/EPSCs) in layer V pyramidal cells of neocortex and transitional cortex (e.g. medial prefrontal, cigulate and frontoparietal). The EPSCs were suppressed by LY293558, an antagonist selective for the AMPA subtype of excitatory amino acid receptor, and by two selective 5-HT2A receptor antagonists, MDL 100907 and SR 46349B. In addition, the EPSCs were suppressed by the fast sodium channel blocker tetrodotoxin (TTX) and were dependent upon external calcium. However, despite being TTX-sensitive and calcium dependent, there was no evidence that the EPSPs resulted from an increase in impulse flow in excitatory neuronal afferents to layer V pyramidal cells. The EPSCs could be induced rapidly by the microiontophoresis of 5-HT directly to "hot spots" within the apical (but not basilar) dendritic field of recorded neurons, indicating that excitatory amino acids may be released by a TTX-sensitive focal action of 5-HT on a subset of glutamatergic terminals in this region. Consistent with such a presynaptic action, the inhibitory metabotropic glutamate receptor agonist (1S,3S)-aminocyclopentane-1,3-dicarboxylate markedly reduced the induction of EPSPs by 5-HT. Postsynaptically, 5-HT enhanced a subthreshold TTX-sensitive sodium current, potentially contributing to an amplification of EPSC amplitudes. These data suggest 5-HT. via 5-HT2A receptors, enhances spontaneous EPSPs/EPSCs in neocortical layer V pyramidal cells through a TTX-sensitive focal action in the apical dendritic field which may involve both pre- and postsynaptic mechanisms.

Amphetamines↗
PubMed1993

[The effect of a magnesium-free solution on the parameters of the spontaneous excitatory postsynaptic potentials in identified snail neurons].

This investigation has revealed that application of magnesium-free medium to snail brain preparation changes the parameters of excitatory input to the identified neurons of the snail: the distribution of amplitude and intervals between EPSP. The other parameters (time to peak level and duration of EPSP) remained unaltered. It is concluded that spontaneous firing activity of initially silent neurons in magnesium-free solution develops as a result of increased efficiency of excitatory input.

Animals↗
PubMed1994

Reduction of perineal evoked excitatory postsynaptic potentials in cat lumbar and sacral motoneurons during micturition.

These experiments were undertaken to examine whether both premotoneuronal mechanisms and direct actions on motoneurons could contribute to suppression of excitatory perineal reflex pathways during micturition. Intracellular recordings were obtained from motoneurons innervating the external urethral sphincter (EUS), external anal sphincter (EAS), and selected hindlimb muscles in decerebrate male cats. The peak amplitudes of EPSPs evoked by electrical stimulation of peripheral cutaneous afferents were measured during micturition. In the EUS, EAS, and hindlimb motoneurons examined, EPSPs produced by stimulation of perineal afferents (superficial perineal or sensory pudendal nerves) were reduced in amplitude during micturition. The sample of PSPs evoked by stimulation of hindlimb cutaneous nerves recorded in hindlimb motoneurons revealed that these PSPs could also be reduced. In contrast, no changes were seen in monosynaptic EPSPs evoked by muscle afferent stimulation. The present study demonstrates that during micturition there is a strong suppression of perineal reflexes to both sphincter and hindlimb motoneurons. Since reduced EUS activity is required for efficient micturition, suppression of the strong excitatory perineal input to EUS motoneurons likely contributes to decreased EUS activity during the bladder contraction. It appears that the micturition circuitry utilizes both premotoneuronal mechanisms and direct motoneuronal inhibition to achieve this reflex suppression. The function of the micturition-related reduction of perineal reflexes to hindlimb or EAS motoneurons is not known at this time and further investigations are required to elucidate the interaction between micturition circuitry and hindlimb cutaneous pathways.

Afferent Pathways↗
PubMed1984

Neuromuscular transmission in the visceral muscle of locust oviduct.

Innervation of the locust oviduct has been investigated with morphological and electrophysiological methods. Using Co2+ and Ni2+ labelling technique, it was found that G7 N2B1 and B2a nerves innervate the oviduct musculature. Ultrastructurally two different terminals could be distinguished: (a) nerve endings containing mainly clear vesicles forming neuromuscular junctions with the muscle fibers; and (b) nerve terminals containing electron-dense granules which showed only "synaptoid" structures, but failed to form junctions with the muscle cells. The neuromuscular junctions proved to be functioning, since it was possible to record intracellularly miniature excitatory postsynaptic potentials and excitatory postsynaptic potentials from the muscle cells. The distribution of the amplitudes of the miniature excitatory postsynaptic potentials suggests a multiterminal innervation. Following electrical stimulation of N2B nerve, excitatory postsynaptic potentials similar to those appearing spontaneously could be evoked. After repetitive stimulation, facilitation or summation of excitatory postsynaptic potentials was observed. The results obtained show that locust oviduct muscle has a double, motor and modulatory innervation.

Animals↗
PubMed1991

Short-latency excitatory postsynaptic potentials are evoked in primate spinothalamic tract neurons by corticospinal tract volleys.

The responses of 8 wide-dynamic-range (WDR) STT neurons to electrical stimulation of the sensorimotor cortex or the cerebral peduncle were recorded intracellularly in anesthetized monkeys. EPSPs and spikes were evoked in STT neurons with short latencies ranging from 0.4 to 5.3 msec after the corticospinal volley, indicating a monosynaptic connection in at least some STT neurons. Spatial and temporal summation seem necessary for the cortex to maintain an effective excitatory influence on STT neurons. It is postulated that the cortical facilitation of STT neurons helps them to acquire more nociceptive signals during behavioral tasks such as exploring a new object so that the brain can make decisions about whether to continue or to abandon a certain task. Possible implications for central pain states are discussed.

Animals↗