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PubMed1987

Excitatory postsynaptic potentials in neonatal rat sympathetic preganglionic neurons: possible mediation by NMDA receptors.

Excitatory postsynaptic potentials (EPSPs) evoked in antidromically identified sympathetic preganglionic neurons (SPNs) and membrane depolarizations induced by N-methyl-D-aspartate (NMDA) applied by pressure ejection were increased by removing Mg ions from the perfusing media and blocked by D-2-amino-5-phosphonovalerate (APV), DL-APV and ketamine. Further, the amplitude of EPSPs and NMDA-induced depolarizations were decreased and increased by membrane hyperpolarization in Krebs solution with and without Mg2+, respectively. These findings indicate that the excitatory amino acid receptor mediating the EPSPs in SPNs may be of the NMDA subtype.

Animals↗
PubMed1976

Analysis of the slow excitatory postsynaptic potential in bullfrog sympathetic ganglion cells.

The ionic mechanism of the slow excitatory postsynaptic potential (slow EPSP), i.e. the muscarinic action of acetylcholine (ACh), was studied either by stimulating preganglionic nerves or by applying ACh in curarized sympathetic ganglion cells of bullfrogs. There are three different types of cells characterized by the effects of membrane hyperpoliarization on the amplitude of slow EPSP. One group of cells showed an increase in amplitude (type 1 cell) and, in two other groups of cells, it remained unchanged (type 2 cell) or decreased (type 3 cell), when the membrane was hyperpolarized. Under the muscarinic effects of ACh, the slope membrane conductance was increased (type 1 cell), unchanged (type 2 cell) or decreased (type 3 cell) at 10-20 mV hyperpolarized levels, while it was unchanged (type 1 cell) or decreased (types 2 and 3 cells) at resting and depolarized levels. In all cells, the slow ACh potential, corresponding to the slow EPSP, was almost completely suppressed in a high K+, Ca2+-free, Na+-free solution. These results suggest that the slow EPSP is generated by increases in Na+ and Ca2+ conductance and also by a simultaneous decrease in the K+ conductance.

Acetylcholine↗
PubMed1992

Quantal parameters of "minimal" excitatory postsynaptic potentials in guinea pig hippocampal slices: binomial approach.

Binomial distributions of amplitudes of excitatory postsynaptic potentials (EPSPs) mixed with Gaussian noise were simulated. The objective of Monte Carlo simulations was, firstly, to study influences of sampling size (N) and noise standard deviation (Sn) on estimates of mean quantal content (m), quantal size (v) and binomial parameters (n and p) by four methods of quantal analysis (histogram, variance, failures and combined method) based on the binomial model and, secondly, to modify these methods on the basis of comparison of estimated with simulated parameters. Reliable estimates (within +/- 10% of the simulated values) were obtained for large sample sizes (N = 500-1000) with Sn less than or equal to v by the histogram (deconvolution) method and with Sn less than or equal to 2v by the other three methods. Similar results were obtained by averages from about 10 simulations if smaller samples were used (N = 50-200). In electrophysiological experiments on slices, "minimal" EPSPs were recorded from CA1 pyramidal cells after low-intensity stimuli to stratum radiatum or stratum oriens. Amplitudes of minimal EPSPs fluctuated in a manner predicted by the quantum hypothesis. Amplitude distributions of EPSPs in the non-facilitated state were adequately described either by binomial statistics with an average p equal to about 0.4 (a range of 0.3-0.7) and an average n of about 3 (range 2-6) or by Poisson statistics with m of about 1. The quantal analysis suggests that typical values of m and v for a single activated fibre in stratum radiatum might be about 0.5-1 and 300-400 microV, respectively, with low p (0.1-0.3) and n (2-4). However, the estimates of binomial parameters should be considered as coarse approximations in view of the simulation results and a possible nonuniformity of parameter p. The comparison of results of various methods based on the binomial model, in both simulation and physiological experiments, indicates the reliability of estimates of basic quantal parameters (m and v) under realistic conditions of physiological experiments. The methods are considered to be sufficiently sensitive to make use of them for studies on mechanisms of long-term synaptic plasticity.

Animals↗
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↗
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↗
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↗
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↗
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↗
PubMed1982

Quantal analysis of excitatory postsynaptic potentials induced in hippocampal neurons by activation of granule cells.

The values of quantal content (m) and quantal amplitude (q) of excitatory postsynaptic potentials (EPSPs) elicited in CA3 neurons by activation of granule cells were estimated in thin hippocampal sections maintained in vitro. For this purpose, DL-homocysteate was administered to granule cells, and trains of EPSPs that were typical for single granule cell activation were recorded from individual CA3 neurons. The amplitudes of the first and second EPSPs in each train were measured. Fron the mean and variance of the amplitude of the EPSPs, the values of q and m were calculated. The values of m and q for the first EPSPs were estimated at 8.3 and 0.28 mV, respectively, on the average. Potentiation of the second EPSPs was accompanied by a two-fold increase in the values of m without changes in the values of q. Therefore, frequency potentiation in synapses between mossy fibers and CA3 neurons may be explained by an increase in number of released quanta. Amplitudes of EPSPs were found to fluctuate in a manner described by Poisson's law.

Animals↗
PubMed1989

Kynurenic acid antagonizes the excitatory postsynaptic potential elicited in neostriatal neurons in the in vitro slice of the rat.

Stimulation of corpus callosum in rat brain slices evoked an excitatory postsynaptic potential (EPSP) in neostriatal neurons. This EPSP is greatly reduced by exposing the slice to kynurenic acid (KY). The action of KY is reversed when the preparation is bathed in normal Ringer's solution. KY reduces the EPSP amplitude in a dose-dependent fashion, with 1 mM KY attenuating the potential by 86%. The effect is not due to a conductance change, since KY treatment does not alter the neuron's input resistance.

Action Potentials↗
PubMed1989

Reduction by general anaesthetics of group Ia excitatory postsynaptic potentials and currents in the cat spinal cord.

1. The effects of thiopentone and halothane on excitatory synaptic transmission at group Ia afferent synapses on lumbosacral motoneurones were studied in the anaesthetized or decerebrate cat. 2. Thiopentone (10 mg kg-1) infused on a background of light pentobarbitone anaesthesia caused a decrease in single-fibre monosynaptic group Ia excitatory postsynaptic potentials (EPSPs) of between 0 and 24%. A step increase in inspired halothane concentration in the range 0.7-0.9% produced a decrease in EPSP amplitude of between 0 and 31%. These effects were reversible when the anaesthetic level was reduced. 3. Fluctuation analysis of selected single-fibre group Ia EPSPs revealed that these effects could be accounted for by a decrease in the probability of occurrence of EPSPs of larger amplitude, and an increase in the probability of occurrence of EPSPs of smaller amplitude. The mean separation between discrete amplitudes was not altered by either anaesthetic agent. 4. EPSPs whose time course indicated a somatic site of origin were voltage clamped to study the effect of the anaesthetics on the time course of the synaptic currents. Neither thiopentone nor halothane produced a consistent effect on the time constant of decay of the current, although they both depressed its peak amplitude. 5. The results are interpreted as indicating a presynaptic site of action of both anaesthetics at the concentrations studied: the probability of release of neurotransmitter is reduced, without any detectable change in the mean duration of the postsynaptic conductance increase. These findings are discussed in relation to the mechanisms of action of anaesthetics on exocytosis and presynaptic inhibition.

Animals↗
PubMed1986

Partitioning of monosynaptic Ia excitatory postsynaptic potentials in the motor nucleus of the cat lateral gastrocnemius muscle.

Experiments were conducted to test the hypothesis that a partitioning of Ia monosynaptic excitatory postsynaptic potentials (Ia EPSPs) is present in motor nuclei supplying muscles with regions capable of different mechanical actions. Intracellular recordings of synaptic potentials were made in lateral gastrocnemius (LG) motoneurons in anesthetized low-spinal cats. The effects were tested of stimuli (group I range) to the four primary nerve branches of the LG nerve supplying muscle compartments LGm, LG1, LG2, and LG3 (terminology of English, Ref. 26) and the nerve to a heteronymous muscle, soleus. Stimulation of a given LG nerve branch produced monosynaptic Ia EPSPs of greater amplitude in "own-branch" motoneurons than "other-branch" cells. A significant partitioning of mean Ia EPSPs was found in three (LG1, LG2, LG3) out of the four homonymous pathways studied. An EPSP normalization (7) was performed to eliminate potential differences in cell type that might affect the amplitudes of the EPSPs between these four cell groups (e.g., differences in the number of cells supplying FF, FR, and S muscle units). This normalization confirmed that the partitioning of monosynaptic Ia inputs upon stimulation of LG1, LG2, and LG3 could not be attributed to differences in cell type. In addition, the effects of LGm stimulation were found to be significantly greater in the LGm motoneurons compared with the other cell groups. Heteronymous input (from soleus) to the LG motor nucleus showed some partitioned effects. Motoneurons innervating compartment LG2 received larger EPSPs from soleus than did the cells supplying compartments LG1, LG3, and LGm. The contributions of location specificity and species specificity (terminology of Scott and Mendell, Ref. 55) in the establishment of these Ia-afferent-motoneuronal connections were examined. Cell location sites within the spinal cord were consistent with location specificity making some contribution to the observed pattern of homonymous Ia connections. A more prominent role for species specificity was indicated by species-dependent differences in EPSP amplitude in pairs of LG motoneurons (e.g., LGm vs. LG2) at similar rostrocaudal locations upon stimulation of a given homonymous or heteronymous nerve/branch.

Afferent Pathways↗
PubMed1985

Synaptic transmission between dorsal root ganglion and dorsal horn neurons in culture: antagonism of monosynaptic excitatory postsynaptic potentials and glutamate excitation by kynurenate.

Intracellular recording techniques have been used to provide information on the identity of excitatory sensory transmitters released at synapses formed between dorsal root ganglion (DRG) and dorsal horn neurons maintained in cell culture. Explants of embryonic rat DRG were added to dissociated cultures of embryonic dorsal horn neurons and synaptic potentials were recorded intracellularly from dorsal horn neurons after DRG explant stimulation. More than 80% of dorsal horn neurons within 1 mm of DRG explants received at least one fast, DRG-evoked, monosynaptic input. In the presence of high divalent cation concentrations, the acidic amino acid receptor agonists, L-glutamate, kainate, and quisqualate excited all dorsal horn neurons which received a monosynaptic DRG neuron input, whereas aspartate and N-methyl-D-aspartate (NMDA) had little or no action. Several compounds reported to antagonize the actions of acidic amino acids were tested for their ability to block DRG-evoked synaptic potentials and glutamate-evoked responses in dorsal horn neurons. 2-Amino-5-phosphonovalerate, a selective NMDA receptor antagonist, was relatively ineffective at antagonizing DRG-evoked synaptic potentials and glutamate-evoked responses. In contrast, kynurenate was found to be a potent antagonist of amino acid-evoked responses and of synaptic transmission at all DRG-dorsal horn synapses examined. The blockade of synaptic transmission by kynurenate appeared to result from a postsynaptic action on dorsal horn neurons. These findings indicate that glutamate, or a glutamate-like compound, but not aspartate, is the excitatory transmitter that mediates fast excitatory postsynaptic potentials at the DRG-dorsal horn synapses examined in this study.

Animals↗
PubMed1992

Excitatory postsynaptic potentials recorded from regular-spiking cells in layers II/III of rat sensorimotor cortex.

1. Intracellular recording techniques were used to investigate the physiological and pharmacological properties of stimulus-induced excitatory postsynaptic potentials (EPSPs) recorded in regular-spiking cells located in layers II/III of rat sensorimotor cortical slices maintained in vitro. 2. Depending on the strength of the extracellular stimuli, a pure EPSP or an EPSP-inhibitory postsynaptic potential sequence was observed under perfusion with normal medium. The EPSPs displayed short latency of onset [2.4 +/- 0.7 (SD) ms] and were able to follow repetitive stimulation (tested less than or equal to 5 Hz). Variation of the membrane potential (Vm) revealed two types of voltage behavior for the short-latency EPSP. The first type decreased in amplitude with depolarization and increased in amplitude with hyperpolarization. In contrast, the second type behaved anomalously by increasing and decreasing in size after depolarization and hyperpolarization, respectively. 3. Several experimental procedures were carried out to investigate the mechanism underlying the anomalous voltage behavior of the EPSP. Results indicated that this type of Vm dependency could be mimicked by an intrinsic response evoked by a brief pulse of depolarizing current and could be abolished by N-(2,6-dimethylphenylcarbamoylmethyl)triethylammonium bromide (50 mM). Furthermore, the EPSP was not sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP, 10 microM). Thus the anomalous voltage relationship of the neuronal membrane. 4. The involvement of non-NMDA receptors in excitatory synaptic transmission was investigated with their selective antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 1-10 microM). This drug greatly reduced or completely blocked the EPSP in a dose-dependent manner (1-10 microM). The IC50 for the CNQX effect was approximately 2 microM. In the presence of CNQX (10 microM) and glycine (10 microM), synaptic stimulation failed to elicit firing of action potential. However, a CPP-sensitive EPSP was observed. 5. When synaptic inhibition was reduced by low concentration of bicuculline methiodide (BMI, 1-2 microM), extracellular stimulation revealed late EPSPs (latency to onset: 10-30 ms) that were not discernible in normal medium. Similar to the short-latency EPSP, the Vm dependency displayed by this late EPSP could be modified by inward membrane rectifications. The late EPSP appeared to be polysynaptic in origin because 1) its latency of onset was long and variable and 2) it failed to follow repetitive stimuli delivered at a frequency that did not depress the short-latency EPSP.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMedDate not supplied

[Electrotonic excitatory postsynaptic potentials evoked by stimulation of ventral roots in motoneurons and Muller axons of Lampetra fluviatilis lampreys].

In experiments on isolated spinal cord of the lamprey, during stimulation of the ventral roots, excitatory postsynaptic potentials (EPSP) in motonuerons and Muller axons were recorded which are stable to the abssence of Ca and the presence of Mg in the perfusion fluid. With the increase in stimulation the EPSP gradually increased, persisting after the subtraction of extracellular field from the recorded intracellular response. The results obtained demonstrate that in the lamprey excitation may be transmitted electrotonically from activated motoneurons to the adjacent ones and to Muller axons. It is suggested that neighbour motoneurons interact via electric synapses which are formed by the returning collaterals of motor axons and by motoneurons, as well as via dendro-dendritic contacts.

Aminopyridines↗
PubMed1992

Activation of kappa-opioid receptors depresses electrically evoked excitatory postsynaptic potentials on 5-HT-sensitive neurones in the rat dorsal raphé nucleus in vitro.

Intracellular recordings from dorsal raphé neurones in slices from rat brains were used to study the actions of kappa-opioid receptor agonists on an excitatory postsynaptic potential (epsp) evoked by local electrical stimulation of afferent terminals. The epsp was observed on all 5-HT-sensitive neurones and was blocked by 1 microM TTX. The epsp was reduced in a dose-dependent manner by the specific kappa-opioid receptor agonist [5R-(5 alpha,7 alpha,8 beta)]-N-methyl-N-[7-(1-pyrrolidinyl)-1- oxaspiro[4.5]dec-8-yl]-4-benzofuranacetamide monohydrochloride (CI-977) (1-100 nM). The effects of CI-977 were blocked by the specific kappa-opioid receptor antagonist norbinaltorphimine (NorBNI) (0.1-1 microM). In the presence of the GABAA receptor antagonists picrotoxin and bicuculline (30 microM), CI-977 still had its depressant action on the epsp. Application of the excitatory amino acid receptor antagonists either kynurenic acid (0.5-1 mM) or 6-cyano-2,3-dihydro-7-nitro-quinoxaline-2,3-dione (CNQX) (30 microM) and DL-2-amino-5-phosphonovaleric acid (APV) reduced both the peak and area of the epsp suggesting that the main component of the epsp evoked by electrical stimulation was largely due to release of excitatory amino acids from afferent terminals. Using potassium chloride-filled recording electrodes an epsp which was only partially occluded by kynurenic acid or CNQX and APV was seen on some neurones, this residual epsp was insensitive to CI-977 but was blocked by 30 microM picrotoxin and bicuculline. The specific mu-opioid receptor agonist, DAGOL, had no consistent effect on the fast epsp. Longer duration electrical stimuli produced a slow inhibitory postsynaptic potential (ipsp) and a long duration increase in firing. CI-977 did not affect either the slow 5-HT-mediated ipsp which was blocked by spiperone or the slow noradrenaline-mediated increase in firing which was sensitive to prazosin. CI-977 did not change the depolarizing response to brief applications of either glutamic acid or N-methyl-D-aspartic acid (NMDA). CI-977, NorBNI, naloxone, DAGOL, picrotoxin, bicuculline and kynurenic acid had no consistent effects on the resting postsynaptic membrane potential or conductance. Under voltage-clamp conditions CI-977 had no effect on a membrane current resembling IA. These results suggest that kappa-opioid receptors are present on the terminals of afferents which release excitatory amino acids onto the 5-HT-sensitive neurones in the raphé.

2-Amino-5-phosphonovalerate↗
PubMed1990

N-methyl-D-aspartate receptors contribute to excitatory postsynaptic potentials of cat lateral geniculate neurons recorded in thalamic slices.

Neurons of the cat's dorsal lateral geniculate nucleus were recorded intracellularly to study the contribution of N-methyl-D-aspartate (NMDA) receptors to excitatory postsynaptic potentials (EPSPs) and low-threshold calcium spikes. EPSPs were evoked by stimulation of retinogeniculate axons in the optic tract and/or corticogeniculate axons in the optic radiations; EPSPs from both sources were similar. These EPSPs had one or two components, and the second component had several characteristics of NMDA receptor-mediated events. For example, EPSP amplitude decreased when neurons were hyperpolarized and increased when stimulus frequency was increased; these EPSPs could also be blocked reversibly by application of the selective NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV). We also studied the influence of NMDA receptors on low-threshold calcium spikes, which are large, voltage- and calcium-dependent depolarizations that are often accompanied by high-frequency action potential discharge. APV blocked synaptically activated low-threshold calcium spikes, but APV had no effect on low-threshold calcium spikes that were elicited by current injection. Therefore, APV does not appear to have a direct effect on the T-type calcium channel that is involved in generation of low-threshold calcium spikes. The voltage and frequency dependence of the NMDA receptor-mediated component of the EPSPs, as well as its ability to trigger low-threshold calcium spikes, provide for complex signal processing in the lateral geniculate nucleus.

2-Amino-5-phosphonovalerate↗
PubMed1987

Delta-opioid receptors mediate inhibition of fast excitatory postsynaptic potentials in cat parasympathetic colonic ganglia.

1 The effects of opioids on synaptic transmission in cat sacral parasympathetic colonic ganglia were studied in vitro, using intracellular electrophysiological techniques. Electrical stimulation of the pelvic nerve evoked fast excitatory postsynaptic potentials (e.p.s.ps), which were blocked by hexamethonium and tetrodotoxin. 2 [D-Pen2, D-Pen5] enkephalin and [Met5]enkephalinamide, delta-opioid receptor agonists, caused concentration-dependent, reversible depression of fast e.p.s.ps, but had no effect on depolarizations evoked by pressure ejection of the nicotinic agonist 1,1-dimethyl-4-phenyl-piperazinium. Cell transmembrane potential and membrane input resistance were also unaffected. 3 U-50,488H, a kappa-opioid receptor agonist, had a very small depressant action while [D-Ala2, MePhe4, Gly-ol5] enkephalin, a mu-opioid receptor agonist, had no effect on fast e.p.s.p. amplitude. Neither compound affected cell transmembrane potential or membrane input resistance. 4 The inhibitory actions of [D-Pen2, D-Pen5] enkephalin were antagonized by both naloxone, an antagonist at each of the three opioid receptor types, and by ICI 174,864, an antagonist selective for delta-opioid receptors. 5 Naloxone and ICI 174,864 both also potentiated fast e.p.s.p. amplitude per se in 50% of cells tested. 6 It is concluded that exogenous opioids act at presynaptic delta-opioid receptors to inhibit sacral parasympathetic synaptic transmission in cat colonic ganglia in vitro. Furthermore, the effects of opioid antagonists alone, suggest that endogenous opioids may also be released by preganglionic nerve stimulation and so regulate the release of acetylcholine in these ganglia.

Animals↗