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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↗

PubMed1995

All-or-none excitatory postsynaptic potentials in the rat visual cortex.

Intracellular recordings were obtained from supragranular neurons in slices of the rat visual cortex. In approximately 25% of the cells large (0.5-1.6 mV) excitatory postsynaptic potentials (EPSPs) of constant amplitude were observed after minimal, presumably single-fibre stimulation. The amplitude variance of these large EPSPs was surprisingly small and within the range of the variance of the noise. These EPSPs could be reduced in amplitude by paired-pulse and low-frequency stimulation or by raising extracellular Mg2+ concentration. Reduced EPSPs could either continue to behave as all-or-none responses, or they could fluctuate between several amplitude levels. Conversely, responses where the amplitude fluctuated from trial to trial under control conditions could be converted into large all-or-none responses by paired-pulse facilitation. This indicates that the large all-or-none EPSPs were composed of several subunits, probably reflecting the action of several different release sites. It is concluded that these release sites are either independent and operate with a probability close to 1 or, if operating with a lower probability, are coordinated by a mechanism which synchronizes release. Several observations suggest that release probabilities can switch from values close to 1 to 0 with repetitive stimulation or high Mg2+ concentration. Thus, a substantial fraction of single-fibre inputs to supragranular cells possess synapses which operate with high synaptic efficiency and extremely low variance under control conditions but can undergo drastic changes in efficacy when release probabilities are interfered with. Such modifications of release probability could serve as an effective mechanism to regulate the gain of synaptic transmission.

Animals↗

PubMed1999

Long-term depression of perforant path excitatory postsynaptic potentials following synchronous network bursting in area CA3 of immature hippocampus.

Various forms of synaptic long-term potentiation and depression have been studied in detail in hippocampus and neocortex. Each are produced by specific patterns of synaptic activation and rely on electrical stimulation of afferents for their induction. Few studies have explored the ability of activity produced by cortical networks themselves to generate similar long-term changes in synaptic efficacy. Experiments have shown that periods of synchronized network bursting in both slices and dissociated cultures of hippocampus can lead to persistent network discharges. Conversely, one study has reported that network discharging can disrupt the induction of long-term potentiation in hippocampus. Whether long-term depression can be induced by synchronous network discharging is unknown. In experiments reported here, we examined the long-term effects of synchronized activity within hippocampal CA3 networks on synaptic potentials produced by the converging perforant path. Prior to induction of network bursting, slices were incubated in a perfusate containing picrotoxin and elevated (4 mM) Ca2+ and Mg2+. To induce network discharges, the concentration of both divalent cations were reduced to normal levels (1.5 mM). Following 20 min of network bursting, perforant path synapses, that did not participate in network discharging, underwent a 30% non-decrementing long-term depression. At the same time, synchronized network discharges, that were absent prior to induction, persisted upon return to preinduction conditions. The antagonist of the N-methyl-D-aspartate receptor, D(-)2-amino-5-phosphonovalerate, blocked both long-term depression of perforant path excitatory postsynaptic potentials and persistent network discharging. Results suggest that activity generated by hippocampal networks is able to produce long-term depression of non-coincidentally active synapses.

2-Amino-5-phosphonovalerate↗

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↗

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↗

PubMed1994

A characterization of excitatory postsynaptic potentials in the avian nucleus magnocellularis.

1. The activation of current-clamped neurons in the chick nucleus magnocellularis (nMAG) by eighth nerve stimulation has been studied in a brain slice preparation using patch electrodes. Single presynaptic stimuli produced rapidly rising, suprathreshold, excitatory postsynaptic potentials (EPSPs) with a synaptic delay of approximately 0.4 ms. Spontaneous, miniature EPSPs (mEPSPs) were evident in control extracellular solution and in the presence of tetrodotoxin (TTX). 2. The EPSP was composed of a large, brief component that was sensitive to antagonists of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, and a smaller, slowly decaying component that was sensitive to both N-methyl-D-aspartate (NMDA) and AMPA receptor antagonists. 3. Injection of depolarizing current steps revealed a strong outward rectification of the membrane conductance at potentials close to the resting potential. Consequently, neurons could fire only a single, TTX-sensitive action potential during a current step. The conductance responsible for this rectification was sensitive to 1 mM 4-aminopyridine but not to 1 mM tetraethylammonium. 4. Following the termination of depolarizing current pulses, membrane potential decayed with a half-time (t1/2) that decreased as the depolarizing current increased, reaching approximately 0.25 ms for a depolarization from rest of 20 mV. The t1/2 for the decay of EPSPs matched the membrane t1/2, indicating that the underlying synaptic conductance decays more quickly than the membrane t1/2. 5. The slow phase of the EPSP was always longer than the membrane t1/2 and increased in size with hyperpolarization. This result is consistent with the contribution of AMPA receptors to the slow, as well as fast, EPSP. 6. The safety factor for transmission with low-frequency stimuli was large, as indicated by the rise time of the EPSP, the extent to which the EPSP shunted the action potential, and the size of EPSPs after prolongation of the synaptic conductance by cyclothiazide. 7. During repetitive synaptic stimulation, the slow EPSPs summated to produce a plateau depolarization of 10-20 mV. The plateau potential was only partially blocked by NMDA receptor antagonists. 8. During trains of stimuli, the faster EPSPs rode atop the plateau potential and could drive action potentials at rates up to 500 Hz for short periods. Synaptic depression was evident during trains, such that EPSPs often fell below threshold after 5-10 stimuli at rates above 200 Hz. EPSPs could remain suprathreshold for several seconds at 50 Hz.(ABSTRACT TRUNCATED AT 400 WORDS)

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↗

PubMed1994

Calcium transients in dendrites of neocortical neurons evoked by single subthreshold excitatory postsynaptic potentials via low-voltage-activated calcium channels.

Simultaneous recordings of membrane voltage and concentration of intracellular Ca2+ ([Ca2+]i) were made in apical dendrites of layer 5 pyramidal cells of rat neocortex after filling dendrites with the fluorescent Ca2+ indicator Calcium Green-1. Subthreshold excitatory postsynaptic potentials (EP-SPs), mediated by the activation of glutamate receptor channels, caused a brief increase in dendritic [Ca2+]i. This rise in dendritic [Ca2+]i was mediated by the opening of low-voltage-activated Ca2+ channels in the dendritic membrane. The results provide direct evidence that dendrites do not function as passive cables even at low-frequency synaptic activity; rather, a single subthreshold EPSP changes the dendritic membrane conductance by opening Ca2+ channels and generating a [Ca2+]i transient that may propagate towards the soma. The activation of these Ca2+ channels at a low-voltage threshold is likely to influence the way in which dendritic EPSPs contribute to the electrical activity of the neuron.

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↗

PubMed1996

4(R)- and 4(S)-(5-phenylpentyl)-glutamic acids attenuate excitatory postsynaptic potential on hippocampus without inhibiting postsynaptic NMDA and AMPA receptors.

The electrophysiological effects of 4(R)- and 4(S)-(5-phenylpentyl)-glutamic acids (C5R and C5S analogues) were investigated. In the presence of 5 microM C5R or C5S, excitatory postsynaptic potentials (EPSPs), elicited by stimulating the Schaffer collateral-commissural pathway, recorded in the hippocampal CA1 region on rat brain slices were reduced by more than 50% of the control. Both the NMDA receptor- and the non-MNDA receptor-mediated components of the EPSP were attenuated to the similar extent. The blockade of the presynaptic input, by 0.5 microM tetrodotoxin (TTX), resulted in that C5 analogues no longer inhibited the depolarization induced by AMPA or NMDA on brain slices. On the other hand, the AMPA- and NMDA-induced whole cell inward current of the dissociated hippocampal neurons was not affected by the presence of C5 analogues, investigated with the whole cell patch-clamping technique. These results suggest that the site of the inhibitory action of C5R and C5S may be at the presynaptic termini and that the release of the excitatory neurotransmitter, most likely the glutamate, may be tampered.

Animals↗

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↗