SEARCH · PubMed Health

Results for “Excitatory Postsynaptic Potentials”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 73 records · Page 4Linked to original sources

PubMed2002

17beta-Estradiol reduces excitatory postsynaptic potential (EPSP) amplitude in rat basolateral amygdala neurons.

We examined the actions of estrogen on excitatory synaptic transmission in the basolateral amygdala (BLA), a brain region involved in learning, emotions, and the effects of stress. Intracellular recordings of monosynaptic excitatory postsynaptic potentials (EPSPs) were obtained from BLA neurons in a slice preparation. Bath application of 17beta-estradiol (2 micro M) reduced EPSP amplitude by an average of 77%. This reduction was readily reversed by washing with control saline and was not mimicked by the inactive isomer 17 alpha-estradiol. Other passive and active properties of BLA neurons were unaffected by 17beta-estradiol. The observed EPSP reduction is in sharp contrast to the potentiation of EPSPs by estrogen observed in other brain regions.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1990

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

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

Acetylcholine↗

PubMed1997

Contribution of metabotropic glutamate receptors to the depression of excitatory postsynaptic potentials during hypoxia.

We tested the hypothesis that activation of metabotropic glutamate receptors (mGluR) might contribute to the depression of excitatory postsynaptic potentials during hypoxia. The experiments were performed on hippocampal slices taken from young (12-14 days old) Wistar rats. The depression induced by hypoxia (14 min) was not modified in the presence of either the non-selective mGluR antagonist (which blocks mainly group I and II mGluR), MCPG (500 microM) or the selective group III mGluR antagonist, MPPG (500 microM). However, in experiments performed in the presence of the selective adenosine A1 receptor antagonist, DPCPX (50 nM), part of the hypoxia-induced depression could be prevented by MPPG (500 microM). Activation of group III mGluR may contribute to the hypoxia-induced depression, but this contribution is only revealed when adenosine A1 receptors are blocked.

Alanine↗

PubMed1998

Active summation of excitatory postsynaptic potentials in hippocampal CA3 pyramidal neurons.

The manner in which the thousands of synaptic inputs received by a pyramidal neuron are summed is critical both to our understanding of the computations that may be performed by single neurons and of the codes used by neurons to transmit information. Recent work on pyramidal cell dendrites has shown that subthreshold synaptic inputs are modulated by voltage-dependent channels, raising the possibility that summation of synaptic responses is influenced by the active properties of dendrites. Here, we use somatic and dendritic whole-cell recordings to show that pyramidal cells in hippocampal area CA3 sum distal and proximal excitatory postsynaptic potentials sublinearly and actively, that the degree of nonlinearity depends on the magnitude and timing of the excitatory postsynaptic potentials, and that blockade of transient potassium channels linearizes summation. Nonlinear summation of synaptic inputs could have important implications for the computations performed by single neurons and also for the role of the mossy fiber and perforant path inputs to hippocampal area CA3.

Animals↗

PubMed1983

Adaptive changes in firing rates in goldfish auditory fibers as related to changes in mean amplitude of excitatory postsynaptic potentials.

Relationship between the firing rate in the auditory fibers and the amplitude of the excitatory postsynaptic potentials (EPSPs) that trigger afferent impulses was investigated. The unitary EPSPs and spike potentials were extracellularly recorded from the goldfish large auditory fibers by means of a microelectrode placed close to the distal terminals. The relation between the firing rate and the amplitude of the EPSPs was studied using a variety of stimulus conditions. The firing probability of phase-locked impulses was linearly related to the mean amplitude of the EPSPs determined for the same time bins. The same linear relation was applicable for the firings elicited by different intensities of sound and observed at various times after onset and also for the firings produced by applying step increments in intensity. The threshold amplitude of the EPSPs required for initiation of afferent impulses was unchanged in these different situations. Random changes in the amplitude of successively evoked EPSPs were found to underlie the probabilistic nature of the sequence of afferent firings. The present results indicate that the per stimulus adaptation and incremental and decremental responses, as observed in the firing probability of afferent impulses, are largely attributable to adaptive changes in the mean amplitude of the evoked EPSPs and not to changes in excitability of the auditory fibers.

Adaptation, Physiological↗

PubMed1999

Gamma-Hydroxybutyrate inhibits excitatory postsynaptic potentials in rat hippocampal slices.

Gamma-Hydroxybutyrate (GHB) has been shown to mimic different central actions of ethanol, to suppress alcohol withdrawal syndrome, and to reduce alcohol consumption both in rats and in humans. The aim of the present study was to determine if GHB shared with alcohol the ability to inhibit glutamate action at both NMDA and AMPA/kainate receptors. The NMDA or the AMPA/kainate receptors-mediated postsynaptic potentials were evoked in CA1 pyramidal neurons by stimulation of Schaffer-collateral commissural fibers in the presence of CGP 35348, bicuculline to block the GABA(B) and GABA(A) receptors, and 10 microM 6,7-dinitroquinoxaline-2,3-dione (DNQX) or 30 microM DL-2-amino-5-phosphonovalerate (d-APV) to block AMPA/kainate or NMDA receptors, respectively. GHB (600 microM) produced a depression of both NMDA and AMPA/kainate receptors-mediated excitatory postsynaptic potentials with recovery on washout. The GHB receptors antagonist, NCS-382, at the concentration of 500 microM had no effect per se on these responses but prevented the depressant effect of GHB (600 microM) on the NMDA and AMPA/kainate-mediated responses. In the paired-pulse experiments, GHB (600 microM) depressed the amplitude of the first and the second evoked AMPA/kainate excitatory postsynaptic potentials, and significantly increased the paired-pulse facilitation (PPF). These results suggest that GHB inhibits excitatory synaptic transmission at Schaffer-collateral commissural-pyramidal neurons synapses by decreasing the probability of release of glutamate.

2-Amino-5-phosphonovalerate↗

PubMed1984

Attenuation of glutamate-action, excitatory postsynaptic potentials, and spikes by intracellular QX 222 in hippocampal neurons.

The effects of intracellular applications of QX 222, a quaternary analogue of lidocaine, were investigated in CA1 neurons of in vitro hippocampal slices of guinea-pig brain. QX 222 produced a strong depression of spontaneous, electrically-(by current injection) or orthodromically-evoked action potentials. These dose-dependent effects were characterized by a reduction in the rate of rise and amplitude of spikes, presumed to be mediated by a Na+-conductance. Although resting membrane conductance tended to diminish with prolonged applications of QX 222, marked changes in resting potential generally were not observed. The threshold for eliciting spikes by intracellular injection of depolarizing current was increased greatly by QX 222, reflecting the impairment of Na+-electrogenesis of spikes. The reduction of action potential amplitude by QX 222 may be partly attributable to enhanced inactivation of Na+-channels because brief depolarizing pulses preceded by strong tonic hyperpolarization, elicited spikes at a lower threshold and of considerably larger amplitude than in the absence of such tonic hyperpolarization. These observations on recovery are compatible with a removal of sodium inactivation. However, this experimental paradigm of current injection also might be expected to remove QX 222 molecules from their blocking sites at the inner end of Na+-channels. When spikes were abolished by QX 222, the depolarization evoked with application of S-glutamate by pressure ejection from an extracellular micropipette positioned close to the neuron was attenuated. This reversible blockade was reproducible in the 14 neurons where the interactions of QX 222 and glutamate were examined systematically. Excitatory postsynaptic potentials, evoked by stimulation of strata oriens or radiatum, were reduced in a similar manner by internal QX 222. These data confirm previous observations that voltage-dependent Na+-channels mediating spike genesis in CA1 neurons can be blocked by internal QX 222. However, QX 222 also apparently interferes with the functions of Na+-channels activated by glutamate-receptor interaction or by receptor interactions with neurotransmitter(s) associated with certain excitatory postsynaptic potentials in CA1 neurons.

Action Potentials↗

PubMed1997

Purinergic fast excitatory postsynaptic potentials in myenteric neurons of guinea pig: distribution and pharmacology.

BACKGROUND & AIMS: Adenosine triphosphate (ATP) acting at P2 receptors mediates some fast excitatory postsynaptic potentials (fEPSPs) in myenteric neurons of guinea pig ileum. The present studies investigate the distribution of purinergic fEPSPs along the length of the gut and characterize the P2-receptor subtype mediating fEPSPs. METHODS: Conventional intracellular electrophysiological methods were used to record from myenteric neurons in vitro. RESULTS: At a membrane potential of -97 +/- 1 mV, the amplitude (25 +/- 1 mV; n = 307) of fEPSPs was similar along the gut. Hexamethonium (100 micromol/L) inhibited fEPSPs in the gastric corpus by 98% +/- 1% (n = 31) and in the duodenum, ileum, taenia coli, proximal colon, and distal colon by 42%-55%. In the presence of hexamethonium, suramin (100 micromol/L) or the P2X antagonist pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 10 micromol/L) reduced the control fEPSP amplitude in the duodenum, ileum, taenia coli, proximal colon, and distal colon by 71%-84%. The pharmacology of the purinergic fEPSPs was investigated in detail in the ileum. Noncholinergic fEPSPs were concentration-dependently (1-30 micromol/L) inhibited by PPADS (50%-inhibitory concentration, 3 micromol/L). In addition, alpha,beta-methylene 5'-adenosine triphosphate (1 micromol/L) also reduced purinergic fEPSPs. CONCLUSIONS: Fast EPSPs mediated in part through P2X receptors are prominent in myenteric neurons along the small and large intestines but are rare in the gastric corpus.

Adenosine Triphosphate↗

PubMed2001

Presynaptic modulation by group III metabotropic glutamate receptors (mGluRs) of the excitatory postsynaptic potential mediated by mGluR1 in rat cerebellar Purkinje cells.

Purkinje neurons were recorded from rat cerebellar slices. Parallel fibres stimulation elicited a fast excitatory postsynaptic potential (EPSP) mediated by ionotropic glutamate (iGluR) -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors followed by the inhibitory gamma-aminobutyric acidA (GABAA)-dependent postsynaptic potential. In the presence of antagonists for iGluRs and for GABAA receptors, brief tetanic activation evoked a slow metabotropic glutamate receptor (mGluR)-dependent EPSP (mGluR-EPSP). This mGluR-EPSP was blocked by the selective mGluR1 antagonists LY367385 and CPCCOEt, but not by the mGluR5 antagonist MPEP. Group II agonists affected neither iGluR-EPSP nor mGluR-EPSP. Conversely, L-AP4 and L-SOP, group III mGluR agonists, inhibited both iGluR- and mGluR-EPSPs. The depolarisations evoked by both AMPA and group I agonists were unaffected, indicating a presynaptic action of group III mGluRs. These data suggest that glutamate released by parallel fibres activates group III mGluR autoreceptors, depressing both iGluR- and mGluR1-mediated EPSPs.

Animals↗

PubMed2003

Active decay of composite excitatory postsynaptic potentials in hippocampal slices from young rats.

NMDA receptor dependent synaptic plasticity was examined in hippocampal slices using a novel pharmacological pairing procedure. Field excitatory postsynaptic potentials (EPSPs) were recorded from the CA1 area of slices maintained in a low Mg(2+) solution using a stimulus rate of 0.1-0.2 Hz. The NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP5) was initially included in the perfusion solution to establish baseline recording of isolated AMPA EPSPs. Washing out AP5 led to the expression of composite EPSPs, containing both AMPA and NMDA receptor mediated components. Following an initial, transient potentiation of the AMPA component, the composite responses gradually decayed for several hours, involving AMPA and NMDA components to a similar extent. This decay was input specific and could be terminated at any stage by reapplication of AP5. Subsequent long-term potentiation (LTP) reversed the effect to an extent inversely related to the degree of depression. Experiments to test the interaction with long-term depression (LTD) revealed a significant but incomplete overlap between the two depression processes. In conclusion, pairing synaptic activation at test stimulus frequency with pharmacological unblocking of NMDA receptors allows for expression of composite EPSPs that decay substantially, due to an active mechanism. The underlying process appears to be at least partly distinct from those involved in homosynaptic LTP and LTD.

Age Factors↗

PubMedDate not supplied

High potency of the orally-active NMDA-receptor antagonist CGP 40 116 in inhibiting excitatory postsynaptic potentials of rat basolateral amygdala neurones in vitro.

Conventional intracellular recordings were used to monitor postsynaptic potentials of basolateral amygdala neurones (BLA) in brain slices comprising the BLA, the entorhinal cortex (EC) and the hippocampus, in which the EC-BLA connections were preserved. Stimulation of the BLA with a bipolar electrode elicited complex postsynaptic potentials consisting of alpha-amino-3-hydroxy-5-methyl-isoxazoleproprionic acid (AMPA) receptor-mediated fast excitatory postsynaptic potentials (fast EPSPs), gamma-amino-butyric acid [GABA(A)] receptor-mediated fast inhibitory postsynaptic potentials (fast IPSPs) and GABAB receptor-mediated slow IPSPs. Bath application of 10 microM of the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and of 10 microM of the GABA(A) receptor antagonist bicuculline methiodide (BMI) revealed a N-methyl-D-aspartate (NMDA) receptor-mediated slow EPSPs, which was occasionally followed by a GABAB receptor-mediated slow IPSPs. Under these conditions, the log concentration-response curve for D-(E)-2-amino-4-methyl-5-phosphono-3-pentanoic acid (CGP 40 116), a newly developed drug with proposed NMDA-receptor antagonist properties, was compared to that obtained with the 'classic' antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) in inhibiting the NMDA-mediated postsynaptic potentials. CGP 40 116 (IC50: 130 nM) was over 30 times more potent than D-AP5 (IC50: 4100 nM) in reducing NMDA-mediated slow EPSP. In conclusion, the present study indicates that CGP 40 116, a new orally-active NMDA antagonist, shows a very high potency on NMDA receptors in the amygdala and may therefore be a valuable tool for studying the behavioural effect of NMDA-receptor mediated transmission in this structure.

2-Amino-5-phosphonovalerate↗

PubMed1979

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

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

Animals↗

PubMed1993

Enhancement of monosynaptic excitatory postsynaptic potentials by glutamate in frog spinal motoneurons.

We analyzed glutamate-induced enhancement of the amplitude of monosynaptic excitatory postsynaptic potentials evoked by stimulation of the lateral column fibers (LC-EPSPs) on lumbar motoneurons in the frog spinal cord. Low concentrations (0.1-0.3 mM) of glutamate, which produced small depolarization, often enhanced EPSP associated with inhibition of a paired pulse facilitation and increased occurrence of spontaneous EPSPs. With 1 mM glutamate, transient enhancement of EPSP was seen in some cells during the early phase or prior to large depolarization, even when input conductance was increased. Transient or sustained enhancement of EPSP was occasionally seen with N-methyl-D-aspartate, kainate and quisqualate, but not with L-2-amino-4-phosphonobutyrate. The results suggest that glutamate enhanced release of excitatory transmitters at low concentrations that apparently did not affect the postsynaptic membrane.

Animals↗

PubMed2000

The involvement of adenosine neuromodulation in pentobarbital-induced field excitatory postsynaptic potentials depression in rat hippocampal slices.

We investigated the contribution of adenosine neuromodulation to mechanisms of pentobarbital-induced depression of excitatory synaptic transmission in vitro. Transverse hippocampal slices were prepared from brains removed from isoflurane-anesthetized male Wistar rats. Field excitatory postsynaptic potentials (fEPSPs), elicited by orthodromic electrical stimulation of Schaffer collateral at 0.05 Hz, were recorded from the CA1 region in oxygenated artificial cerebrospinal fluid. Amplitude of fEPSP was analyzed for assessing drug effects. Pentobarbital (100 microM) transiently depressed fEPSPs (P<0.01); i.e., fEPSP was initially depressed to approximately 60% of control and then recovered to approximately 80% of control. The fEPSP depression was partially suppressed by pretreatment with 50 microM aminophylline, a nonselective adenosine receptor antagonist, and 0.2 microM 3, 7-Dimethyl-1-propagylxanthine, an adenosine A(1) receptor antagonist (P<0.01 each). However, the fEPSP depression was not affected by pretreatment with 10 microM 8-cyclopentyl-1, 3-dipropylxanthine, an A(2) receptor antagonist, or 10 microM bicuculline, a gamma-aminobutyric acid (GABA) A receptor antagonist. The results indicate that adenosine neuromodulation through A(1) receptors and other undefined mechanisms, which are independent from GABAergic mechanisms, are involved in pentobarbital-induced depression of excitatory synaptic transmission.

Adenosine↗

PubMed1992

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

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

Animals↗

PubMed1996

Gamma-hydroxybutyric acid decreases thalamic sensory excitatory postsynaptic potentials by an action on presynaptic GABAB receptors.

The effect of gamma-hydroxybutyric acid (GHB) on the excitatory postsynaptic potential (EPSP) evoked in thalamocortical neurones of the rat dorsal lateral geniculate nucleus and ventrobasal thalamus was investigated in vitro. GHB (0.1-5 mM) dose-dependently and reversibly decreased (36-78%) the amplitude of the sensory EPSP. This effect of GHB was blocked by the GABAB receptor antagonist CGP 35348 (1 mM). NCS 382 (1-3 mM), a putative GHB receptor antagonist, did not antagonise but weakly potentiated both the GHB- and baclofen-mediated decrease of the EPSP amplitude.

Adjuvants, Anesthesia↗

PubMed1997

Recurrent excitatory postsynaptic potentials induced by synchronized fast cortical oscillations.

Gamma frequency (about 20-70 Hz) oscillations occur during novel sensory stimulation, with tight synchrony over distances of at least 7 mm. Synchronization in the visual system has been proposed to reflect coactivation of different parts of the visual field by a single spatially extended object. We have shown that intracortical mechanisms, including spike doublet firing by interneurons, can account for tight long-range synchrony. Here we show that synchronous gamma oscillations in two sites also can cause long-lasting (>1 hr) potentiation of recurrent excitatory synapses. Synchronous oscillations lasting >400 ms in hippocampal area CA1 are associated with an increase in both excitatory postsynaptic potential (EPSP) amplitude and action potential afterhyperpolarization size. The resulting EPSPs stabilize and synchronize a prolonged beta frequency (about 10-25 Hz) oscillation. The changes in EPSP size are not expressed during non-oscillatory behavior but reappear during subsequent gamma-oscillatory events. We propose that oscillation-induced EPSPs serve as a substrate for memory, whose expression either enhances or blocks synchronization of spatially separated sites. This phenomenon thus provides a dynamical mechanism for storage and retrieval of stimulus-specific neuronal assemblies.

Animals↗

PubMed2002

Enhancement of N-methyl- D-aspartate receptor-mediated excitatory postsynaptic potentials in the neostriatum after methamphetamine sensitization. An in vitro slice study.

It has been suggested that behavioral methamphetamine sensitization involves changes in cortical excitatory synaptic inputs to neostriatal (Str) projection neurons. To test this, we performed blind whole-cell recording of medium spiny neurons in Str slice preparations. In Str neurons of naive rats, the amplitude of the subcortical white matter stimulation-induced N-methyl- D-aspartate receptor-mediated excitatory postsynaptic potentials (NMDA-EPSPs) was decreased upon hyperpolarization, owing to the voltage-dependent Mg(2+) blockade of NMDA receptor channels. In contrast, the amplitude of the NMDA-EPSPs in Str neurons of rats undergoing methamphetamine withdrawal (MW) did not show the Mg(2+) blockade and was nearly voltage independent over the membrane potential range of -70 to -110 mV. Application of the specific protein kinase C (PKC) activator, phorbol 12, 13- DL-acetate, blocked the voltage-dependent Mg(2+) blockade of NMDA receptor channels in Str neurons of naive rats. Application of the specific activator of cAMP-dependent protein kinase A (PKA), Sp-cAMPS-triethylamine salt, increased the amplitude of the NMDA receptor-mediated EPSPs at the rest but not at hyperpolarized potentials. Coapplication of the PKC and PKA activators yielded NMDA-EPSPs similar to those seen in Str neurons of MW rats. In Str slices of naive rats, tetanic subcortical white matter stimulation induced long-term depression of field potentials. In Str slices treated with the PKC and/or PKA, the same stimulation induced long-term potentiation of field potentials similar to those observed in slices obtained from MW rats. These results suggest that the enhancement of the NMDA receptor-mediated corticostriatal synaptic transmission plays an important role in behavioral methamphetamine sensitization. This enhancement is probably associated with phosphorylation of NMDA receptors mediated by the simultaneous activation of PKC and PKA.

Animals↗