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Results for “Excitatory Postsynaptic Potentials”

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PubMed1977

[Excitatory postsynaptic potentials in the lumbar motor neurons of frogs induced by stimulation of muscle and cutaneous nerves].

The postsynaptic effects evoked in lumbar motoneurons by stimulation of different muscle and cutaneous nerves of hindlimbs were studied by means of intracellular recording in the frog isolated spinal cord. The data obtained confirm presence of monosynaptic connections between primary afferents and spinal motoneurons. Monosynaptic EPSPs were shown to be due to low threshold muscle afferent volleys in homonymous nerves and did not generate spike discharges. The mean amplitude of monosynaptic EPSPs was 1.1 +/- 0.12 mV, time-to-peak 1.76 +/- 0.16 msec, time constant of decay from 6.0 to 15.0 msec. EPSPs with no synaptic delay were recorded in some motoneurons which suggest existence of an electrical mechanism of transmission.

Animals↗
PubMed1990

[The effect of glycine and gamma-aminobutyric acid on the excitatory postsynaptic potentials of the spinal motor neurons in the lamprey in the presence of antagonists].

Effect of bath application of the inhibitory amino acids (glycine and GABA) on motoneurons of EPSPs was studied in the normal physiological solutions and after preliminary administration of antagonists: strychnine (10(-6) mol/l), bicuculline (10(-4) mol/l) or picrotoxin (10(-4) mol/l). All these antagonists diminished the depression of monosynaptic EPSPs which were elicited by both amino acids (glycine and GABA). Data obtained in this study and previously reported ones permit concluding that motoneuron membranes in the spinal cord of lamprey possess the unit receptor channel complex sensitive to both amino acids.

Animals↗
PubMed1988

Synaptic transmission mediated by single club endings on the goldfish Mauthner cell. II. Plasticity of excitatory postsynaptic potentials.

Simultaneous pre- and postsynaptic intracellular recordings were used to analyze the properties of chemically mediated synaptic transmission between single club endings of eighth nerve afferents and the goldfish Mauthner (M-) cell lateral dendrite. The EPSPs exhibited pronounced facilitation when the presynaptic fiber fired high-frequency bursts of 2 or 3 impulses at intervals of 2-4 msec. The amplitudes of the EPSPs evoked by the second and third presynaptic impulses of a burst were, on average, 99 and 108% larger than that evoked by the first impulse. A cross-correlation analysis showed that the amplitudes of the control and facilitated EPSPs fluctuated independently, indicating that the facilitation was mediated by a presynaptic mechanism. This conclusion was supported by a comparison of the coefficient of variation for the control and facilitated EPSPs, on the basis of a binomial release model. In addition, the value of binomial n, the number of presynaptic release units, was not changed during facilitation. The origin of EPSP fluctuations was analyzed by examining the correlation between the amplitudes of EPSPs and those of the electrotonic coupling potentials associated with them. The absence of correlation between the 2 variables suggested that the fluctuations of EPSPs were not due to a variable presynaptic impulse invasion. The EPSP fluctuations were further analyzed by assuming that the facilitation was associated with an increase in the probability (p) of transmitter release and that the release process followed simple binomial statistics. The binomial variables thus calculated were n = 6-11, p = 0.29-0.44, and q = 31-61 microV, values comparable to the estimates for other CNS synapses. More importantly, these parameters provided satisfactory fits to the amplitude histograms of the control and facilitated EPSPs. The number of release units, n, was smaller than, but in a range similar to, the number of active zones identified in the freeze-fracture study of the club endings (Kohno and Noguchi, 1986). This correlation is consistent with the notion that active zones are the structural correlates of quantal release units. In the preceding paper, it was shown that impulses in a majority of club endings electrotonically coupled to the M-cell do not produce a detectable chemically mediated EPSP, although the contacts have the morphological correlates of chemical synapses. In an attempt to activate these "silent" connections, 2 approaches were used. First, the burst-firing paradigm, which could effectively facilitate EPSPs already present, failed to reveal any EPSPs at the silent junctions.(ABSTRACT TRUNCATED AT 400 WORDS)

Algorithms↗
PubMed1980

[Excitatory postsynaptic potentials in motor neurons of rats upon stimulation of individual reticulospinal neurons].

Unit reticulo-motoneuronal EPSPs evoked by extra -- or intracellular stimulation of reticulo-spinal neurons were recorded intracellularly from rat lumbar motoneurons. Reticular neurons with fast conducting axons revealed higher probability of direct effect on motoneurons. Terminals of single reticular neurons to different motoneurons were shown to be widely distributed. Analysis of the time course of average unit EPSPs suggests proximal to soma location of some reticulo-motoneuronal synapses. Amplitude-frequency histograms of the unit EPSPs could be fitted in most cases by Poisson's or binominal distribution, suggesting the quantal nature of transmitter release.

Animals↗
PubMed1981

[Properties of the slow excitatory postsynaptic potential in mammalian sympathetic ganglia neurons].

Slow EPSPs evoked in the neurons of the rabbit isolated superior cervical ganglion were studied using intracellular microelectrodes. Two types of EPSPs occurring in different neurons were found. The type I slow EPSPs showed an increase during hyperpolarization of the membrane and a decrease during its depolarization. Input resistance of the neurons during the response either decreased or remained unchanged. The type II slow EPSPs were increased by depolarization and decreased by hyperpolarization with the reversal potential -78.9 +/- 3.6 mV. Depolarization evoked by acetylcholine or carbocholine was followed by an increase in the input resistance in 53% of neurons with reversal potential -83.2 +/- 6.7 mV. It is concluded that in the first group of the neurons the nature of the slow EPSP is similar to that of ordinary EPSP. The main component underlying the ionic mechanism of slow EPSP in the other group of the neurons is a decrease in potassium conductance of the membrane.

Acetylcholine↗
PubMed1984

Cortically induced postsynaptic potentials in hypoglossal motoneurons after axotomy.

Cortically induced postsynaptic potentials were studied in normal and axotomized cat hypoglossal motoneurons. In normal protruder motoneurons innervating tongue protruder muscles, we have demonstrated that stimulation of the orbital gyrus, at the point optimum for inducing lapping movements of the tongue by repetitive stimuli, produced inhibitory postsynaptic potentials or excitatory postsynaptic potentials followed by predominant inhibitory postsynaptic potentials. The cortically induced excitatory postsynaptic potential in normal protruder motoneurons was composed of only the short-latency component. In protruder motoneurons 30, 40, 60 and 80 days after axotomy, we have demonstrated that the number of protruder motoneurons responding with two components of excitatory postsynaptic potentials (the short- and the long-latency component) to cortical stimulation increased in correspondence with the lapse of days after axotomy and that the amplitude of cortically induced inhibitory postsynaptic potentials in axotomized protruder motoneurons was reduced in size as compared with normal protruder motoneurons.

Animals↗
PubMed2000

Calcium channels controlling acetylcholine release from preganglionic nerve terminals in rat autonomic ganglia.

Little is known about the nature of the calcium channels controlling neurotransmitter release from preganglionic parasympathetic nerve fibres. In the present study, the effects of selective calcium channel antagonists and amiloride were investigated on ganglionic neurotransmission. Conventional intracellular recording and focal extracellular recording techniques were used in rat submandibular and pelvic ganglia, respectively. Excitatory postsynaptic potentials and excitatory postsynaptic currents preceded by nerve terminal impulses were recorded as a measure of acetylcholine release from parasympathetic and sympathetic preganglionic fibres following nerve stimulation. The calcium channel antagonists omega-conotoxin GVIA (N type), nifedipine and nimodipine (L type), omega-conotoxin MVIIC and omega-agatoxin IVA (P/Q type), and Ni2+ (R type) had no functional inhibitory effects on synaptic transmission in both submandibular and pelvic ganglia. The potassium-sparing diuretic, amiloride, and its analogue, dimethyl amiloride, produced a reversible and concentration-dependent inhibition of excitatory postsynaptic potential amplitude in the rat submandibular ganglion. The amplitude and frequency of spontaneous excitatory postsynaptic potentials and the sensitivity of the postsynaptic membrane to acetylcholine were unaffected by amiloride. In the rat pelvic ganglion, amiloride produced a concentration-dependent inhibition of excitatory postsynaptic currents without causing any detectable effects on the amplitude or configuration of the nerve terminal impulse. These results indicate that neurotransmitter release from preganglionic parasympathetic and sympathetic nerve terminals is resistant to inhibition by specific calcium channel antagonists of N-, L-, P/Q- and R-type calcium channels. Amiloride acts presynaptically to inhibit evoked transmitter release, but does not prevent action potential propagation in the nerve terminals, suggesting that amiloride may block the pharmacologically distinct calcium channel type(s) on rat preganglionic nerve terminals.

Acetylcholine↗
PubMed1994

A rise in postsynaptic Ca2+ potentiates miniature excitatory postsynaptic currents and AMPA responses in hippocampal neurons.

We have investigated the site of expression of the potentiation of excitatory postsynaptic currents (EPSCs) induced by the activation of postsynaptic voltage-sensitive Ca2+ channels, by examining the effect of depolarizing pulses on miniature (m) EPSCs and responses to AMPA. Application of voltage pulses caused a approximately 2.5-fold increase in the mean amplitude of mEPSCs. This NMDA receptor-independent potentiation of mEPSC amplitudes was transient, returning to control values within 30-40 min. The potentiation was associated with a decrease in the number of small amplitude events and an increase in the number, as well as the maximum amplitude, of the larger events, with no apparent change in mEPSC kinetics. Accompanying the increase in mEPSC amplitudes, there was a 1.6-fold increase in the apparent frequency of events. Voltage pulse-induced potentiation was completely blocked by the inclusion of the Ca2+ chelator BAPTA in the recording pipette. Responses to repeated applications of AMPA were also potentiated following the application of voltage pulses, and the time course of this potentiation was similar to that observed with the mEPSCs. Our data indicate that rises in intracellular Ca2+ that occur independently of NMDA receptor activation can result in a potentiation of quantal size, which is due to an increase in the postsynaptic sensitivity of non-NMDA receptors.

Animals↗
PubMed1985

Postsynaptic blocking of glutamatergic and cholinergic synapses as a common property of Araneidae spider venoms.

Venom effects of eight Araneidae spider species were studied using locust and frog neuromuscular junctions. The spider venoms irreversibly blocked miniature excitatory postsynaptic potentials and excitatory postsynaptic potentials of locust neuromuscular junction. The frog miniature end-plate potentials and end-plate potentials were also blocked, but they recovered upon washing of the preparation with physiological solution.

Animals↗
PubMed1992

Blockade of hippocampal long-term potentiation by saccharin.

Population spikes, population excitatory postsynaptic potentials and intracellular excitatory postsynaptic potentials were recorded in the CA1 area of guinea-pig hippocampal slices in response to low frequency stimulation of the stratum radiatum. Tetanic stimulation of the same afferents during an application of saccharin (10 mM, 10 min) failed to induced a long-term potentiation of the population spike, population excitatory postsynaptic potential and intracellularly recorded excitatory postsynaptic potential. A post-tetanic application of saccharin did not prevent long-term potentiation of the population spike from developing. Saccharin did not change the input resistance, the membrane potential or the ability to induce action potentials in the CA1 neurons. The slope of the intracellular excitatory postsynaptic potentials recorded in normal medium, in normal medium containing 2-amino-5-phosphonovalerate, or in Mg(2+)-free medium containing 6-cyano-7-nitroquinoxaline-2,3-dione was not significantly altered by saccharin. The depolarizations of CAI neurons produced by superfusion of N-methyl-D-aspartate or during a brief tetanic stimulation of the stratum radiation were also not altered by the drug. It therefore appears that saccharin blocks the induction of long-term potentiation by a mechanism that does not involve a blockade of N-methyl-D-aspartate receptors. Application of fluid samples collected from rabbit neocortical surface during a tetanic stimulation of the neocortex caused neurite growth in PC-12 cells, suggesting that growth-related substances were present in the collected samples. If these samples were superfused onto hippocampal slices, long-term potentiation developed. If however, the samples were co-applied with saccharin, neither neurite growth in PC-12 cells nor long-term potentiation in hippocampal slices was observed, raising the possibility that growth-related substances are involved in long-term potentiation.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2000

Norepinephrine facilitates inhibitory transmission in substantia gelatinosa of adult rat spinal cord (part 2): effects on somatodendritic sites of GABAergic neurons.

BACKGROUND: It has been reported previously that norepinephrine, when applied to the spinal cord dorsal horn, excites a subpopulation of dorsal horn neurons, presumably inhibitory interneurons. In the current study, the authors tested whether norepinephrine could activate inhibitory interneurons, specifically those that are "GABAergic." METHODS: A transverse slice was obtained from a segment of the lumbar spinal cord isolated from adult male Sprague-Dawley rats. Whole-cell patch-clamp recordings were made from substantia gelatinosa neurons using the blind patch-clamp technique. The effects of norepinephrine on spontaneous GABAergic inhibitory postsynaptic currents were studied. RESULTS: In the majority of substantia gelatinosa neurons tested, norepinephrine (10-60 microM) significantly increased both the frequency and the amplitude of GABAergic inhibitory postsynaptic currents. These increases were blocked by tetrodotoxin (1 microM). The effects of norepinephrine were mimicked by the alpha1-receptor agonist phenylephrine (10-80 microM) and inhibited by the alpha1-receptor-antagonist WB-4101 (0.5 microM). Primary-afferent-evoked polysynaptic excitatory postsynaptic potentials or excitatory postsynaptic currents in wide-dynamic-range neurons of the deep dorsal horn were also attenuated by phenylephrine (40 microM). CONCLUSION: The observations suggest that GABAergic interneurons possess somatodendritic alpha1 receptors, and activation of these receptors excites inhibitory interneurons. The alpha1 actions reported herein may contribute to the analgesic action of intrathecally administered phenylephrine.

Adrenergic alpha-1 Receptor Agonists↗