Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Excitatory Postsynaptic Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1986

Presynaptic suppression of excitatory postsynaptic potentials in rat ventral horn neurons by muscarinic agonists.

In addition to depolarizing the ventral horn cells including antidromically identified motoneurons in thin transverse neonatal rat spinal cord slice preparations, exogenously applied acetylcholine (ACh) suppressed the amplitude of excitatory postsynaptic potentials (EPSPs) either occurring spontaneously or elicited by stimulation of dorsal rootlets. A reduction of EPSPs could still be detected when the ACh-induced depolarization was nullified by hyperpolarizing current. Atropine but not D-tubocurarine effectively antagonized the depolarization and synaptic depression caused by ACh. While depressing the EPSPs, ACh had no appreciable effect on membrane depolarizations elicited by glutamate. Methacholine mimicked the depolarizing and synaptic depressant effects of ACh. The results suggest that muscarinic agonists inhibit synaptic transmission of ventral horn neurons including motoneurons by a presynaptic mechanism in reducing the output of excitatory transmitters.

Acetylcholine↗
PubMed1992

Presynaptic facilitation of excitatory postsynaptic potential by glucagon in neurons of rat ventromedial hypothalamic slices.

Intracellular recordings were made from neurons in rat ventromedial hypothalamus (VMH), in vitro. Application of glucagon (100 nM to 5 microM) for 2-5 min increased the amplitude of excitatory postsynaptic potential (EPSP) lasting for 10-20 min. Forskolin and 8-bromo-cyclic AMP mimicked glucagon in producing a long-lasting facilitation of the EPSP. These drugs did not affect depolarizing response produced by glutamate. 3-Isobutyl-1-methylxanthine (IBMX) potentiated the time course of glucagon-induced facilitation of the EPSP. These results suggest that glucagon facilitates the EPSP probably by increasing transmitter release through activation of adenylate cyclase.

Animals↗
PubMed1992

Dopamine enhances both electrotonic coupling and chemical excitatory postsynaptic potentials at mixed synapses.

The transmitter dopamine reduces electrotonic coupling between retinal horizontal cells and increases their sensitivity to glutamate. Since in other systems single afferents establish mixed electrotonic and chemical excitatory synapses with their targets, dopamine might be expected there to depress one component of excitation while enhancing the other. This hypothesis was tested by applying dopamine locally in the vicinity of the lateral dendrite of the goldfish Mauthner cell (M cell) and monitoring the composite electrotonic and chemical excitatory postsynaptic potentials and currents evoked by ipsilateral eighth nerve stimulation. Dopamine produces persistent enhancements of both components of the postsynaptic response while it also increases input conductance. All these dopamine actions are prevented by superfusing the brain with saline containing the dopamine D1 receptor antagonist SCH-23390. Postsynaptic injections of the cAMP-dependent protein kinase inhibitor (Walsh inhibitor, or PKI5-24) block the dopamine-induced changes in synaptic transmission, implicating a cAMP-dependent mechanism. Furthermore, there is a dopaminergic innervation of the M cell, as demonstrated immunohistochemically with antibodies against dopamine and the rate-limiting enzyme in its synthetic pathway, tyrosine hydroxylase. Varicose immunoreactive fibers lie in the vicinity of the distal part of the lateral dendrite between the large myelinated club endings that establish the mixed synapses. As determined with electron microscopy, the dopaminergic fibers contain small vesicles, and they do not have synaptic contacts with either the afferents or the M cell, remaining instead in the synaptic bed. Taken together, these results suggest that dopamine released at a distance from these terminals increases the gain of this primary sensory input to the M cell, most likely through a phosphorylation mechanism.

Animals↗
PubMed1989

Large enhancement of excitatory postsynaptic potentials and currents by thyrotropin-releasing hormone (TRH) in frog spinal motoneurones.

Frog spinal motoneurones were studied in vitro under voltage clamp conditions to examine the effect of the peptide thyrotropin-releasing hormone (TRH). TRH (50 microM) produced a small membrane depolarization, without obvious changes in the neuronal conductance or sensitivity to exogenously applied glutamate. These effects were seen regardless of the presence of 1 mM Mg2+ in the bathing solution. Low- and high-threshold excitatory postsynaptic potentials, induced by dorsal root stimulation, were enhanced by TRH. Under voltage clamp, TRH did not change the cell leak conductance while producing a considerable enhancement of polysynaptic current amplitude, particularly when recorded at a rather negative potential level. It is suggested that TRH might potentiate excitatory neurotransmission by facilitating presynaptic release of the excitatory neurotransmitter(s) onto motoneurones.

Action Potentials↗
PubMed1990

Excitatory postsynaptic potentials in rat neocortical neurons in vitro. III. Effects of a quinoxalinedione non-NMDA receptor antagonist.

1. Intracellular microelectrodes were used to obtain recordings from neurons in layer II/III of rat frontal cortex. A bipolar electrode positioned in layer IV of the neocortex was used to evoke postsynaptic potentials. Graded series of stimulation were employed to selectively activate different classes of postsynaptic responses. The sensitivity of postsynaptic potentials and iontophoretically applied neurotransmitters to the non-N-methyl-D-asparate (NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) was examined. 2. As reported previously, low-intensity electrical stimulation of cortical layer IV evoked short-latency early excitatory postsynaptic potentials (eEPSPs) in layer II/III neurons. CNQX reversibly antagonized eEPSPs in a dose-dependent manner. Stimulation at intensities just subthreshold for activation of inhibitory postsynaptic potentials (IPSPs) produced long-latency (10 to 40-ms) EPSPs (late EPSPs or 1EPSPs). CNQX was effective in blocking 1EPSPs. 3. With the use of stimulus intensities at or just below threshold for evoking an action potential, complex synaptic potentials consisting of EPSP-IPSP sequences were observed. Both early, Cl(-)-dependent and late, K(+)-dependent IPSPs were reduced by CNQX. This effect was reversible on washing. This disinhibition could lead to enhanced excitability in the presence of CNQX. 4. Iontophoretic application of quisqualate produced a membrane depolarization with superimposed action potentials, whereas NMDA depolarized the membrane potential and evoked bursts of action potentials. At concentrations up to 5 microM, CNQX selectively antagonized quisqualate responses. NMDA responses were reduced by 10 microM CNQX. D-Serine (0.5-2 mM), an agonist at the glycine regulatory site on the NMDA receptor, reversed the CNQX depression of NMDA responses.(ABSTRACT TRUNCATED AT 250 WORDS)

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

An N-methyl-D-aspartate receptor mediated excitatory postsynaptic potential evoked in subthalamic neurons in an in vitro slice preparation of the rat.

Subthalamic (STH) neurons with slow EPSPs mediated by an N-methyl-D-aspartate (NMDA) receptor were studied in rat brain slice preparation. When STH neurons were intracellularly recorded with KCl-filled electrodes, stimulation of the internal capsule (IC) evoked a short duration depolarization followed by a slow excitatory postsynaptic potential (EPSP) lasting 100-200 ms. The amplitude of the slow EPSP was increased when the neuron was hyperpolarized by a low intensity current injection but was blocked when it was hyperpolarized with strong current. The slow EPSP was reversibly suppressed by application of 30-50 microM DL-2-amino-5-phosphonovareric acid (APV). STH neurons also were recorded, with potassium methylsulfate filled electrodes, in the slice preparation obtained from rats that received chronic knife cuts of the IC at the level of the entopeduncular nucleus. Stimulation of the IC immediately rostral to the STH evoked a fast EPSP followed by a slow EPSP, and IPSPs were largely eliminated in this preparation. The slow EPSP was augmented in MG-free medium and suppressed by 50 microM APV. These results suggest that NMDA receptor mediating slow EPSPs may regulate activities of STH neurons.

2-Amino-5-phosphonovalerate↗
PubMed1986

An analysis of the action of pentobarbitone on the excitatory postsynaptic potentials and membrane properties of neurones in the guinea-pig olfactory cortex.

Intracellular recordings were made from neurones in slices of guinea-pig olfactory cortex maintained in vitro at 37 degrees C. The average membrane potential was 63 +/- 12 mV and the input resistance of these cells was 42 +/- 20 M omega (mean +/- s.d.). Stimulation of the lateral olfactory tract (l.o.t.) generated a transient depolarization in these cells which had the characteristics of an excitatory postsynaptic potential (e.p.s.p.). If the e.p.s.p. was of sufficient amplitude it culminated in an action potential. The e.p.s.p. was potentiated by repetitive stimulation at 10-50 Hz and showed post-tetanic potentiation after a prolonged period of high frequency stimulation (50-100 Hz for 30-60 s). Pentobarbitone (0.1-0.5 mM) depressed the e.p.s.p. reversibly but was without effect on the resting membrane potential, input resistance or time constant of the neurones. Pentobarbitone did not inhibit potentiation of the e.p.s.p. by a preceding conditioning shock. It is concluded that pentobarbitone does not affect the passive membrane properties of neurones in the olfactory cortex. The depressant action of pentobarbitone on synaptic transmission results from a decrease in the amount of transmitter released in response to a nerve impulse, or a decrease in the sensitivity of the postsynaptic membrane to the transmitter or a combination of both effects.

Animals↗
PubMed1979

Measurements of excitatory postsynaptic potentials in the stretch reflex of normal subjects and spastic patients.

The patellar tendon was tapped by random impulses of triangular waveform and motor unit spikes were recorded from the quadriceps femoris muscle. The cross-correlogram of the taps and the motor unit spikes revealed a primary correlation kernel, the width of which was interpreted as an indicator of the mean time-to-peak of excitatory postsynaptic potentials (EPSPs) elicited monosynaptically in an alpha-motoneurone by the triangular taps. The mean time-to-peak was 7.6 +/- 1.3 ms in normal subjects and 9.0 +/- 1.8 ms in spastic patients (P less than 0.005). The prolonged time-to-peak of EPSP in spastic patients is consistent with the hypothesis that as a result of degeneration of the corticomotoneuronal tract the Ia axons sprout and form more synaptic contacts on distal portions of the dendrites of alpha-motoneurones.

Achilles Tendon↗
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↗
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↗
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↗
PubMed1987

Neurokinin A in capsaicin-sensitive neurons of the guinea-pig inferior mesenteric ganglia: an additional putative mediator for the non-cholinergic excitatory postsynaptic potential.

The presence of neurokinin-A-like immunoreactivity in guinea-pig inferior mesenteric ganglia was detected by radioimmunoassay procedures. Pretreating the animals with capsaicin 7 days prior to experimentations reduced the mean content of neurokinin-A-like immunoreactivity by 85% from its control value of 150 +/- 31.3 fmol per ganglion. High-performance liquid chromatography revealed that neurokinin-A-like immunoreactivity was heterogenous as in addition to neurokinin A, peaks corresponding to the amphibian tachykinin eledoisin and to neuropeptide K were detected, and they too were depleted by capsaicin. Electrophysiological studies showed that neurokinin A applied either by superfusion or by pressure ejection evoked a slow depolarization in the majority of inferior mesenteric ganglia neurons in vitro. Neurokinin-A-evoked depolarizations in the majority of cells tested were associated with a small increase in membrane input resistance. However, the responses were increased by membrane hyperpolarization: the extrapolated mean equilibrium potential of neurokinin-A-induced depolarization was -36 mV. Removal of extracellular sodium but not chloride ions suppressed the neurokinin-A-induced depolarization. The slow depolarization elicited either by exogenously applied substance P or by repetitive stimulation of hypogastric nerves was reversibly eliminated in the presence of neurokinin A. Collectively, our studies suggest that neurokinin-A-like immunoreactivity may coexist with substance-P-like immunoreactivity in capsaicin-sensitive fibers in the guinea-pig prevertebral ganglia and that the similarity of the actions of neurokinin A on the one hand and substance P on the other raises the possibility that non-cholinergic excitatory potentials elicited in the inferior mesenteric ganglia may be generated by not one but a number of closely related tachykinins.

Animals↗