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At least 127 records · Page 7Linked to original sources

PubMed1985

Noradrenaline mediates slow excitatory synaptic potentials in rat dorsal raphe neurons in vitro.

Repetitive focal stimulation to the slice surface within the region of the dorsal raphe (DR) nucleus of rat brain elicited a slow excitatory synaptic potential (slow EPSP), which followed a slow inhibitory synaptic potential (slow IPSP) in a majority of the DR neurons. The slow EPSPs were associated with either an increase of a decrease in membrane resistance. Noradrenaline (NA) application caused a membrane depolarization in most of the DR neurons. The NA-induced depolarization was also accompanied by either an increase or a decrease in membrane resistance. Both the slow EPSP and NA-induced depolarization were inhibited by phentolamine and prazosin but not by yohimbine and propranolol. The result suggests that slow EPSPs in rat DR neurons are mediated by NA interacting with an alpha 1-adrenoceptor.

Animals↗

PubMed1992

Evidence for nitric oxide synthase inhibitor-sensitive and insensitive hippocampal synaptic potentiation.

1. Nitric oxide (NO) has been proposed as a retrograde messenger, mediating the postsynaptic to presynaptic transfer of the effects of conditioning stimulation, responsible for the initiation of hippocampal long-term potentiation (LTP). To further test this hypothesis, we inhibited nitric oxide synthase (NOS) to determine whether synaptic potentiation produced by different conditioning stimulus patterns and intensities was differentially affected by reduction of stimulation-dependent NO production. 2. Synaptic potentiation was produced in hippocampal slices from young F-344 rats by two different conditioning stimulation protocols. Conditioning stimuli were delivered to the Schaffer-collateral commissural system, and moderate levels of potentiation of the population excitatory postsynaptic potential (EPSP) in area CA1 were produced by a single 100 Hz, 1-s conditioning train delivered at half-maximal stimulus intensity. Higher levels of potentiation of the population EPSP were obtained by delivering two 100 Hz, 1-s conditioning stimulus trains, with a 60-s intertrain interval, at high stimulus currents. 3. Application of the nitric oxide synthase inhibitors NG-nitro-L-arginine (NOARG; 0.1-200 microM) and NG-monomethyl-L-arginine (NMMA; 100 microM) produced no significant direct effects on synaptic responses. 4. In slices that received a single conditioning stimulus train, both NOARG and NMMA were ineffective in blocking or reducing potentiation at concentrations between 0.1 and 200 microM. In slices receiving the more intense pair of conditioning stimulus trains, levels of potentiation in control slices were higher, and there was a very significant reduction by both NOARG (50 and 100 microM) and NMMA (100 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1983

Blockade of amino acid-induced depolarizations and inhibition of excitatory post-synaptic potentials in rat dentate gyrus.

Excitatory post-synaptic potentials (e.p.s.p.s) evoked by stimulation of the medial perforant path and depolarizations induced by excitatory amino acids were recorded from granule cells in the preparation of the hippocampal slice from the rat. The effects of (+/-)-2-amino-5-phosphonovalerate (APV), gamma-D-glutamylglycine (gamma DGG) and cis-2,3-piperidinedicarboxylate (PDA), antagonists of excitatory amino acids on these phenomena were compared. gamma DGG was the most effective antagonist of the e.p.s.p. Its action was reversible and not associated with any change in the passive membrane properties of the granule cells or in the apparent reversal potential of the e.p.s.p. Quantal analysis showed that the reduction in the e.p.s.p. paralleled the decrease in quantal size rather than quantal content, confirming a post-synaptic site of the action of gamma DGG. The potency of gamma DGG against the exogenous agonists was N-methyl-D-aspartate greater than kainate greater than or equal to quisqualate. APV had very little effect on the e.p.s.p. but was a selective antagonist of N-methyl-D-aspartate-induced depolarizations. PDA depolarized granule cells and increased their membrane input resistance. Although gamma DGG was a potent antagonist of both glutamate- and aspartate-induced depolarizations, no clear pattern of specificity could be found. The action of glutamate was unaffected by APV. These results indicate that the receptor for the transmitter at the synapses formed by the fibres of the perforant path with the granule cells is of the quisqualate and/or kainate type. The present data are consistent with the biochemical evidence that glutamate may be the endogenous transmitter at his synapse.

2-Amino-5-phosphonovalerate↗

PubMed1996

Blockade of isoproterenol-induced synaptic potentiation by tetra-9-aminoacridine in the rat amygdala.

The effects of tetrahydro-9-aminoacridine (THA) on beta-adrenoceptor activation-induced synaptic potentiation were studied in brain slices of the rat amygdala using intracellular recording techniques. To exclude the involvement of N-methyl-D-aspartate (NMDA) receptors, all the experiments were performed in the presence of NMDA receptor antagonist, D-APV (50 microM). Bath application of isoproterenol (Iso; 15 microM) results in a long-lasting enhancement of the amplitude of excitatory postsynaptic potentials (EPSPs) to 200 +/- 6% of baseline. Forskolin, which directly activates adenyl cyclase, produces a similar effect suggesting that Iso may act through a cyclic AMP-dependent mechanism. Pretreatment of the slices with THA (300 microM) completely abolishes the Iso- and forskolin-induced synaptic potentiation. We hypothesize that the locus of THA/beta-adrenoceptor interaction is presynaptic; the underlying mechanism is likely due to THA's depression of transmitter release via a presynaptic blockade of voltage-dependent Ca2+ channels.

Adrenergic beta-Agonists↗

PubMed1998

On the origin of skewed distributions of spontaneous synaptic potentials in autonomic ganglia.

The histograms of spontaneous synaptic potentials at synapses in autonomic ganglia are described by distributions consisting of mixtures of Gaussians, rather than by single Gaussian distributions. The possible origin of these mixed distributions is investigated, using Monte-Carlo simulations of the action of spontaneously released units of transmitter. A single unit of acetylcholine of fixed size, released from an active zone with receptor patches both beneath and adjacent to the zone, does not give rise to the observed histograms. But if the unit is of variable size, consisting of integer multiples of smaller units, and release is from an active zone onto either the receptor patch beneath, or in addition onto adjacent patches, then the histogram is well described by a mixture of Gaussians. However, this explanation is unlikely to be correct as present evidence suggests that in most cases the released unit of transmitter saturates the postsynaptic receptor patch beneath the active zone. The final case considered is where a unit of transmitter is spontaneously released from an active zone, simultaneously with a unit in an adjacent zone less than one micron away. The histogram of potentials then conforms to those observed even when there are differences in the sizes of the receptor patches. It is suggested that this kind of release could provide an explanation for distributions of spontaneous potentials that are mixtures of Gaussians.

Animals↗

PubMed1991

Is synaptic potentiation necessary for the development of kindling?

Field potentials were recorded from the dentate gyrus of freely moving rats to examine the role of synaptic potentiation in the development of seizure susceptibility during rapid kindling. Kindling stimulations (10 Hz for 10 sec) were delivered to the perforant path at every 5 min for 5 or 6 hrs. This procedure produced a sustained depression of excitatory synaptic transmission at the perforant path-granule cell synapse during and after kindling. However, the kindling procedure resulted in the prolongation of afterdischarges and the development of interictal discharges originated from granule cells, indicating an increase in the seizure susceptibility of these neurons. These results indicate that synaptic potentiation is not a critical requirement for an increase in seizure susceptibility during rapid kindling, even if it has a facilitating effect on the development of kindling as suggested in previous studies.

Animals↗

PubMed1999

Gating of BDNF-induced synaptic potentiation by cAMP.

Neurotrophins have been implicated in activity-dependent synaptic plasticity, but the underlying intracellular mechanisms remain largely unknown. Synaptic potentiation induced by brain-derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3',5'-monophosphate (cAMP) signaling. Activators of cAMP signaling alone were ineffective in modifying synaptic efficacy but greatly enhanced the potentiation effect of BDNF. Blocking cAMP signaling abolished the facilitation of BDNF-induced potentiation by presynaptic activity. Thus synaptic actions of BDNF are gated by cAMP. Activity and other coincident signals that modulate cAMP concentrations may specify the action of secreted neurotrophins on developing nerve terminals.

Animals↗

PubMed2005

Coactivation and timing-dependent integration of synaptic potentiation and depression.

Neuronal synaptic connections can be potentiated or depressed by paired pre- and postsynaptic spikes, depending on the spike timing. We show that in cultured rat hippocampal neurons a calcium/calmodulin-dependent protein kinase II (CaMKII)-mediated potentiation process and a calcineurin-mediated depression process can be activated concomitantly by spike triplets or quadruplets. The integration of the two processes critically depends on their activation timing. Depression can cancel previously activated potentiation, whereas potentiation tends to override previously activated depression. The time window for potentiation to dominate is about 70 ms, beyond which the two processes cancel. These results indicate that the signaling machinery underlying spike timing-dependent plasticity (STDP) may be separated into functional modules that are sensitive to the spatiotemporal dynamics (rather than the amount) of calcium influx. The timing dependence of modular interaction provides a quantitative framework for understanding the temporal integration of STDP.

Animals↗

PubMed1990

Endogenous GABA mediates presynaptic inhibition of spontaneous and evoked excitatory synaptic potentials in the rat neostriatum.

The effect of the blockade of the gamma-aminobutyric acid (GABA) uptake system on the amplitude of glutamatergic synaptic potentials was studied by using a corticostriatal slice preparation. Nipecotic acid (0.1-1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3-3 microM). This effect was not blocked by phaclofen (0.5-1 mM). These findings show that phaclofen-insensitive GABAB receptors, activated by endogenous GABA, mediate presynaptic inhibition of cortical glutamatergic inputs in the neostriatum.

Animals↗

PubMed2002

A synaptic potentiation by a protein factor distinct from those induced by neurotrophins.

We report a protein factor(s) contained in the conditioned medium (CM) of the Mg(2+)-free treatment induced the synaptic potentiation. This type of potentiation shared a different pathway from those induced by neurotrophins. Neurotrophins were confirmed to induce a synaptic potentiation in the dissociated chick neurons. Furthermore, K252a, an inhibitor of tyrosine kinase, abolished this potentiation. Nevertheless, the potentiation induced by the CM was not blocked by K252a. In addition, the CM prepared from the chick neurons induced a similar potentiation in rat and mouse neurons. These results suggest that the protein factor is a novel protein molecule for inducing the potentiation and it plays a critical role in the common mechanism for the potentiation between avian and mammal.

Animals↗

PubMed1993

Properties of GABA-mediated synaptic potentials induced by zinc in adult rat hippocampal pyramidal neurones.

1. Intracellular recording techniques were used to study the actions of the transition ion, zinc, on CA1 and CA3 pyramidal neurones in adult rat hippocampal slices. 2. Zinc (300 microM) hyperpolarized pyramidal neurones, increased the membrane excitability and also induced periodic, spontaneous giant depolarizing potentials associated with a conductance increase mechanism. 3. The occurrence of spontaneous giant depolarizations was dependent on the zinc concentration (10 microM-1 mM) with an apparent dissociation constant of 98 microM. The frequency of zinc-induced depolarizations was unaffected by the membrane potential from -50 to -100 mV. 4. Stimulation of the Schaffer collaterals or mossy fibre pathways evoked an excitatory and inhibitory synaptic potential complex. In the presence of zinc, nerve fibre stimulation evoked, in an all-or-none fashion, a giant depolarizing potential with an increased membrane conductance. Both spontaneous and evoked depolarizations were inhibited by 1 microM tetrodotoxin. 5. Evoked giant depolarizations were labile with too frequent stimulation resulting in a failure of generation. A minimum time of 140 s was required between stimuli to ensure successive giant depolarizations. 6. Spontaneous and evoked zinc-induced depolarizing potentials were inhibited by bicuculline (10 microM) or picrotoxin (40 microM) and enhanced by pentobarbitone (100 microM) or flurazepam (10 microM), suggesting that these potentials are mediated by activation of gamma-aminobutyric acidA (GABAA) receptors. 7. Ionophoretic application of GABA produced biphasic responses at -60 mV membrane potential. The reversal potentials for the depolarizing and hyperpolarizing GABA responses were -56 +/- 5 and -66 +/- 8 mV respectively. The giant depolarizations induced by zinc reversed at -57 +/- 4 mV. This suggests a dendritic location for the generation of these potentials. 8. Excitatory amino acid antagonists, 2-amino-5-phosphonovalerate (APV, 40 microM) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) did not affect the amplitude but slightly reduced the frequency of the giant depolarizations. 9. It is concluded that zinc induces a synchronized release of GABA, quite independent of intact excitatory synaptic transmission, which acts on GABAA receptors producing large depolarizing synaptic potentials. This increased level of GABA release may be of physiological and pathological importance since zinc is a naturally occurring metal ion endogenous to the central nervous system.

Action Potentials↗

PubMed1985

The anion selectivity of GABA-mediated post-synaptic potentials in mouse hippocampal cells.

Intracellular recordings were made from CA1 and dentate cells of the mouse hippocampal slice. When potassium acetate was used to fill the electrodes, spontaneous synaptic activity was rarely seen in CA1 or dentate cells. In contrast, when electrodes filled with potassium chloride were used, spontaneous depolarizing post-synaptic potentials (p.s.p.s) were prominent. That these p.s.p.s were mediated by gamma-aminobutyric acid (GABA) was supported by the following: they were blocked by electrophoretic application of bicuculline methiodide; their appearance was associated with the reversal of the evoked GABA-mediated recurrent inhibitory post-synaptic potential (i.p.s.p.) and their appearance was associated with the positive displacement of the reversal potential for the response to GABA applied by electrophoresis close to the cell soma. The interval distribution for the p.s.p.s could not be fitted by a Poisson distribution. The anionic selectivity of the conductance evoked by GABA was investigated by using the potassium salts of a range of anions to fill the electrodes. Depolarizing spontaneous p.s.p.s were seen in all cells impaled with electrodes containing potassium chloride, iodide, bromide, nitrate, or chlorate. In these cells, the reversal potential for the response to electrophoretically applied GABA was displaced in the depolarizing direction and the evoked recurrent i.p.s.p. was reversed. When anions with hydrated shells larger than chlorate (bicarbonate, sulphate, chromate, acetate or citrate) were used, spontaneous depolarizing p.s.p.s were not seen, and the reversal potential for the response to somatic GABA application and for the evoked recurrent i.p.s.p. lay between -70 and -75 mV.

Action Potentials↗

PubMed1986

A magnesium-sensitive post-synaptic potential in rat cerebral cortex resembles neuronal responses to N-methylaspartate.

In isolated slices of rat cerebral cortex, intracellular recordings were obtained from pyramidal cells that were predominantly in layers II/III. These cells could be antidromically activated from the underlying white matter and had resting potentials of greater than -75 mV, action potentials with amplitudes of greater than 70 mV (measured from threshold), overshoots of 20-30 mV, and thresholds 20-30 mV positive to the resting potential. The responses of these cells to short (1-2 s) pulses of electrophoretically applied N-methylaspartate (NMA) decreased in amplitude with membrane hyperpolarization between -40 and -120 mV, and were associated with an apparent increase in membrane resistance when recorded in the presence of 1 mM-Mg2+. However, in the absence of Mg2+, responses to NMA increased progressively in amplitude with hyperpolarization and were associated with a decrease in membrane resistance. In addition to conventional excitatory post-synaptic potentials (e.p.s.p.s) and inhibitory post-synaptic potentials (i.p.s.p.s), electrical stimulation of the underlying white matter evoked a novel e.p.s.p. This e.p.s.p. displayed a similar voltage relation to the response evoked by NMA and was associated with an apparent increase in membrane resistance. When Mg2+ was removed from the bathing medium, the properties of the novel e.p.s.p. changed, and it displayed a conventional voltage relation and was associated with a decrease in membrane resistance. In the absence of Mg2+, novel e.p.s.p.s showed potentiation on low frequency repetitive stimulation (0.5-2 Hz). A fully potentiated response could evoke bursts of slow potentials each of which could evoke a burst of fast spikes. In contrast, the more conventional e.p.s.p.s and i.p.s.p.s evoked in pyramidal neurones were unaffected by reducing the Mg2+ concentration from 1.0 to near 0 mM and conventional e.p.s.p.s showed no potentiation on repetitive, low frequency repetition, even after several hours exposure to Mg2+-free medium. The NMA antagonists: 2-amino-5-phosphonovaleric acid, ketamine and cyclazocine, applied electrophoretically at doses that blocked responses to NMA, but which had little effect on responses to glutamate, blocked the novel e.p.s.p. and its potentiation.

Action Potentials↗

PubMed2002

Post-ischaemic long-term synaptic potentiation in the striatum: a putative mechanism for cell type-specific vulnerability.

In the present in vitro study of rat brain, we report that transient oxygen and glucose deprivation (in vitro ischaemia) induced a post-ischaemic long-term synaptic potentiation (i-LTP) at corticostriatal synapses. We compared the physiological and pharmacological characteristics of this pathological form of synaptic plasticity with those of LTP induced by tetanic stimulation of corticostriatal fibres (t-LTP), which is thought to represent a cellular substrate of learning and memory. Activation of N-methyl-D-aspartate (NMDA) receptors was required for the induction of both forms of synaptic plasticity. The intraneuronal injection of the calcium chelator BAPTA [bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate] and inhibitors of the mitogen-activated protein kinase pathway blocked both forms of synaptic plasticity. However, while t-LTP showed input specificity, i-LTP occurred also at synaptic pathways inactive during the ischaemic period. In addition, scopolamine, a muscarinic receptor antagonist, prevented the induction of t-LTP but not of i-LTP, indicating that endogenous acetylcholine is required for physiological but not for pathological synaptic potentiation. Finally, we found that striatal cholinergic interneurones, which are resistant to in vivo ischaemia, do not express i-LTP while they express t-LTP. We suggest that i-LTP represents a pathological form of synaptic plasticity that may account for the cell type-specific vulnerability observed in striatal spiny neurones following ischaemia and energy deprivation.

Acetylcholine↗

PubMed1993

Pharmacological isolation and characterization of NMDA receptor-mediated synaptic potential in the dentate gyrus of rat hippocampal slices.

We attempted to observe the dentate gyrus field potential evoked by low-frequency stimulation of the perforant path in Mg(2+)-free medium and identify the N-methyl-D-aspartate (NMDA) receptor-mediated synaptic potential using rat hippocampal slices. When perfusing solution was changed from normal medium (1.3 mM Mg2+) to Mg(2+)-free medium, the evoked potential was greatly increased and secondary population spikes appeared following a primary population spike. The evoked potential recorded in Mg(2+)-free medium was only partly blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA receptor antagonist. The CNQX-resistant component of the evoked potential in Mg(2+)-free medium was completely abolished by 30 microM DL-2-amino-5-phosphonovalerate, a NMDA receptor antagonist, indicating that the NMDA receptor-mediated synaptic response can be isolated by masking the non-NMDA receptor-mediated component of the evoked potential under the Mg(2+)-free condition. The isolated NMDA receptor-mediated synaptic potential was also blocked by 7-chlorokynurenate, an antagonist at the glycine site of the NMDA receptor, and restored by the concomitant presence of glycine. Observation of pharmacologically isolated NMDA receptor-mediated synaptic potential is a simple and good method for studying the direct effects of drugs on NMDA receptor-mediated responses.

2-Amino-5-phosphonovalerate↗

PubMed1967

Spontaneous synaptic potentials and quantal release of transmitter in the stellate ganglion of the squid.

1. Several kinds of synapses have been studied in the stellate ganglion of the squid.2. A small electric coupling was found between giant fibres in different stellar nerves.3. Post-synaptic potentials recorded from the cells of small axons are composite, indicating that there are converging inputs from several pre-ganglionic fibres.4. Spontaneous miniature synaptic potentials were recorded from all types of synapses. Miniature potentials in the cells of small axons had a slower time course than those in the giant fibre system.5. Tetrodotoxin abolished nerve impulses in the ganglion but did not prevent the spontaneous quantal release of transmitter from the terminals, or its action on the post-synaptic membrane; nor did it prevent the increase in rate of release produced by depolarization of the presynaptic fibre.6. Glutamate depolarized the giant fibre when applied iontophoretically to the synaptic region. Similar doses applied intracellularly were without effect.

Action Potentials↗

PubMed1971

An electrical description of the motoneurone, and its application to the analysis of synaptic potentials.

1. The Rall model of the motoneurone, which consists of a lumped resistance and capacitance, representing the soma, in parallel with a distributed resistance-capacitance network of finite length, representing the equivalent dendritic cable, has been used to investigate the effects of varying electrical and geometrical parameters on the time course of transients generated at the model soma.2. An analytical solution has been obtained for the voltage at the model soma, following a brief current injection at any point on the dendritic cable, in terms of the dendritic to soma conductance ratio, the electrotonic length of the cable, the membrane time constant, and the electrotonic distance between the point of current injection and the soma. This solution has been used to study the response at the soma to currents with a smooth time course, and to brief rectangular current pulses. Computations of these voltage transients are given to illustrate the effect of the above parameters on voltage time course.3. A method for determining the membrane time constant, the dendritic to soma conductance ratio, and the electrotonic length of the dendritic cable, is described. The method involves measurements from the decay time course of the transient at the soma following a brief current pulse being applied at the soma.4. A method is described whereby the time course of a synaptic potential, assumed to be generated by synaptic knobs located exclusively at the soma, may be used to determine the motoneurone parameters, and a parameter describing the time course of current injection.5. A method for estimating the distance between soma and origin of a non-somatic synaptic potential, once the parameters of the motoneurone are known, is described.

Computers↗

PubMed2001

Synchronized population oscillation of excitatory synaptic potentials dependent of calcium-induced calcium release in rat neocortex layer II/III neurons.

We examined the roles played by calcium-induced calcium release from ryanodine-sensitive calcium stores in induction of neocortical membrane potential oscillation by using caffeine, an agonist of ryanodine receptors. Intracellular recordings were made from neurons in layer II/III of rat visual cortex slices in a caffeine-containing medium. White matter stimulation initially evoked monophasic synaptic potentials. As low-frequency stimulation continued for over 10 min, an oscillating synaptic potential gradually became evoked, in which a paroxysmal depolarization shift was followed by a 8-10-Hz train of several depolarizing wavelets. This oscillating potential was not induced in a medium containing no caffeine with 2 or 0.5 mM [Mg2+](o). Under blockade of N-methyl-D-aspartate receptors, induction of this oscillating potential failed even with caffeine application. Experiments with the calcium store depletor, thapsigargin, revealed that this oscillating potential is induced in a manner dependent on intracellular calcium release. Dual intracellular recordings revealed that the oscillation was synchronized in pairs of layer II/III neurons. The oscillating potential was detectable by field potential recordings also, suggesting that the present oscillation seems to reflect a network property.

Animals↗