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At least 19 recordsLinked to original sources
PubMed1999

Regulation of depolarizing GABA(A) receptor-mediated synaptic potentials by synaptic activation of GABA(B) autoreceptors in the rat hippocampus.

The role of GABA(B) autoreceptors in the regulation of GABA(A) and GABA(B) receptor-mediated inhibitory post-synaptic potentials (IPSPs) during repetitive synaptic activation has been established. In the present study the role of these receptors in the regulation of depolarising GABA(A) receptor-mediated synaptic potentials (DPSP(A)s) in the CA1 region of the hippocampus is documented. Following blockade of AMPA and NMDA receptor-mediated synaptic excitation, DPSP(A)s could be evoked by a single stimulus. The size of this response was enhanced by increasing the stimulus number (1-10 shocks) or stimulus frequency (10-100 Hz). Conversely, the amplitude of the DPSP(A) was dramatically reduced by a priming pulse (single shock) or priming burst (four shocks) delivered 200 ms beforehand. This activity-dependent depression was eliminated by the GABA(B) receptor antagonist CGP 35348 (1 mM). As such, GABA(B) autoreceptor-mediated regulation of DPSP(A)s prevented a pronounced, potentially epileptogenic, DPSP(A) from occurring during theta burst stimulation. Thus, during repetitive stimulation, activation of GABA(B) autoreceptors not only enables a transient reduction in GABA(A) receptor-mediated synaptic inhibition sufficient to enable NMDA receptor-dependent synaptic plasticity [Davies, C.H., Collingridge, G.L., 1996. J. Physiol. 496.2, 451-470] but also prevents the development of a potentially pathogenic depolarising GABA-mediated synaptic potential.

Animals↗
PubMed1991

Voltage-sensitive dye recording of action potentials and synaptic potentials from sympathetic microcultures.

Given the appropriate multicell electrophysiological techniques, small networks of cultured neurons (microcultures) are well suited to long-term studies of synaptic plasticity. To this end, we have developed an apparatus for optical recording from cultured vertebrate neurons using voltage-sensitive fluorescent dyes (Chien, C.-B., and J. Pine. 1991. J. Neurosci. Methods. 38:93-105). We evaluate here the usefulness of this technique for recording action potentials and synaptic potentials in microcultures of neurons from the rat superior cervical ganglion (SCG). After extensive dye screening and optimization of conditions, we chose the styryl dye RH423, which gave fast linear fluorescence changes of approximately 1%/100 mV for typical recordings. The root mean square noise of the apparatus (limited by shot noise) was typically 0.03%, equivalent to 3 mV of membrane potential. Illumination for at least 100 flashes of 100 ms each caused no noticeable photodynamic damage. Our results show that voltage-sensitive dyes can be used to record from microcultures of vertebrate neurons with high sensitivity. Dye signals were detected from both cell bodies and neurites. Signals from presumptive dendrites showed hyperpolarizations and action potentials simultaneous with those in the cell body, while those from presumptive axons showed delayed propagating action potentials. Subthreshold synaptic potentials in the cell body were occasionally detectable optically; however, they were usually masked by signals from axons passing through the same pixel. This is due to the complex anatomy of SCG microcultures, which have many crisscrossing neurites that often pass over cell bodies. Given a simpler microculture system with fewer neurites, it should be possible to use dye recording to routinely measure subthreshold synaptic strengths.

Action Potentials↗
PubMed1995

Cyclic adenosine-3',5'-monophosphate potentiates the synaptic potential mediated by NMDA receptors in the amygdala.

An in vitro slice preparation of rat amygdala was used to study the actions of forskolin and cyclic adenosine-3',5'-monophosphate (cAMP) analogues on the N-methyl-D-aspartate (NMDA) receptor-mediated synaptic potential (EPSPNMDA). Intracellular recordings were made from basolateral amygdala neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-di-one (CNQX, 10 microM) and picrotoxin (50 microM) to pharmacologically isolate the EPSPNMDA. Application of forskolin (25 microM) markedly and persistently potentiated the EPSPNMDA. In contrast, the inactive forskolin analogue, 1,9-dideoxy-forskolin, failed to affect the EPSPNMDA significantly. Superfusion of dibutyryl-cAMP (dbcAMP, 200 microM) for 15 min caused a transient depression of the amplitude of EPSPNMDA. The EPSPNMDA amplitude was reduced to 68 +/- 3% of control (n = 10) 15 min after the application, restored to its control value within 25 min, and followed by a long-term potentiation (LTP). Pretreating the slices with 8-cyclopentyl-1,3-dipropyl-xanthine (DPCPX, 5 microM), a selective A1 receptor antagonist, blocked the transient depressive phase produced by dbcAMP. This result suggests that the transient depression induced by dbcAMP was likely due to the interaction of dbcAMP or its breakdown products with adenosine A1 receptors. To determine the site of action, we examined the effect of forskolin on the postsynaptic responses to exogenously applied NMDA. Forskolin potentiated the postsynaptic depolarization induced by NMDA, suggesting that the enhancement is mediated, at least in part, by a persistent upregulation of postsynaptic NMDA receptor-operated conductances. Occlusion experiments were performed to examine whether the sustained enhancements of EPSP(NMDA) produced by tetanic stimulation (TS) and forskolin share a common mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1999

Anaesthetic/amnesic agents disrupt beta frequency oscillations associated with potentiation of excitatory synaptic potentials in the rat hippocampal slice.

1. Anaesthetic agents produce disruption in cognitive function typified by reductions in sensory perception and memory formation. Oscillations within the EEG gamma and beta bands have been linked to sensory perception and memory and have been shown to be modified by anaesthetic agents. 2. Synchronous gamma oscillations generated by brief tetanic stimulation in two regions of hippocampal area CA1 in slices in vitro were seen to potentiate excitatory synaptic communication between the areas. This synaptic potentiation, was seen to contribute to a transition from gamma frequency (30 - 70 Hz) to beta frequency (12 - 30 Hz) oscillations. 3. Four drugs having anaesthetic/hypnotic and amnesic properties were tested on this synchronous gamma-induced beta oscillation. Thiopental 10 - 200 microM, Diazepam 0.05 - 1.0 microM, Morphine 10 - 200 microM, and Ketamine 10 - 200 microM were all added to the bathing medium. Each drug markedly disrupted the formation of beta oscillations in a manner consistent with their primary modes of action. Thiopental and morphine disrupted synchrony of gamma oscillations and prevented potentiation of recurrent excitatory potentials measured in stratum oriens (fEPSPs). Neither diazepam, nor ketamine produced such marked changes in synchrony at gamma frequencies or reduction in potentiation of fEPSPs. However, each disrupted expression of subsequent beta oscillation via changes in the magnitude of inhibitory network gamma oscillations and the duration and magnitude of tetanus-induced depolarization respectively. 4. The degree of disruption of fEPSP potentiation correlated quantitatively with the degree of disruption in synchrony between sites during gamma oscillations. The data indicate that synchronous gamma-induced beta oscillations represent a mode of expression of excitatory synaptic potentiation in the hippocampus, and that anaesthetic/amnesic agents can disrupt this process markedly.

Anesthetics↗
PubMed1987

Long-lasting potentiation of synaptic potentials in the motor cortex produced by stimulation of the sensory cortex in the cat: a basis of motor learning.

A long-lasting increase in the efficiency of synaptic transmission in the central nervous system has been thought to be one of the bases of learning and memory. To explore the possibility that the motor cortex (area 4 gamma) itself is involved in motor learning, the existence of long-term potentiation (LTP) was examined by recording excitatory postsynaptic potentials (EPSPs) from motor cortical neurons. Short tetanic intracortical microstimulation (ICMS) of the somatic sensory cortex produced a marked potentiation of the EPSPs in a small group of motor cortical neurons. The results raised the possibility that the input from the sensory cortex participates in motor learning and retention of the learned motor skills.

Animals↗
PubMedDate not supplied

Synaptic reliability correlates with reduced susceptibility to synaptic potentiation by brain-derived neurotrophic factor.

Recent studies have implicated brain-derived neurotrophic factor (BDNF) in use-dependent modification of hippocampal synapses. BDNF can rapidly potentiate synaptic transmission at glutamatergic synapses by enhancing transmitter release. Using simultaneous perforated patch recording from pairs and triplets of glutamatergic hippocampal neurons, we have examined how the initial state of the glutamatergic synapse determines its susceptibility to synaptic modification by BDNF. We found that the degree of synaptic potentiation by BDNF depends on the initial reliability and strength of the synapse: Relatively weak connections were strongly potentiated, whereas the effect was markedly reduced at stronger synapses. The degree of BDNF-induced potentiation strongly correlated with the initial coefficient of variation (CV) of the amplitude of excitatory postsynaptic currents (EPSCs) and inversely correlated with the initial paired-pulse facilitation, suggesting that synapses with lower release probability (Pr) are more susceptible to the action of BDNF. To determine whether saturation of Pr could have masked the potentiation effect of BDNF in the stronger synapses, we lowered the initial Pr either by reducing the extracellular Ca2+ concentration ([Ca2+]o) or by bath application of adenosine. Synapses that were initially strong remained unaffected by BDNF under these conditions of reduced Pr. Thus, the lack of BDNF effect on synaptic efficacy cannot simply be accounted for by saturation of Pr, but rather may be due to intrinsic changes associated with synaptic maturation that might covary with Pr. Finally, the dependence on initial synaptic strength was also found for divergent outputs of the same presynaptic neuron, suggesting that synaptic terminals with different degrees of responsiveness to BDNF can coexist within in the same neuron.

Animals↗
PubMed1984

Phenytoin reduces frequency potentiation of synaptic potentials at the frog neuromuscular junction.

The action of the commonly used antiepileptic drug phenytoin on frequency potentials was studied at the frog neuromuscular junction. Whereas the drug, at concentrations of 0.1-0.3 mM, had only a slight effect on EPPs evoked by nerve stimulation at a frequency of 0.5 Hz, it strongly suppressed their potentiation during tetanic nerve stimulation at 30 Hz. The post-tetanic potentiation of the EPPs was also reduced by the drug. These effects occurred without a blockade of invasion of the nerve impulse into the presynaptic terminal during the tetanus, and thus indicate a specific frequency-dependent depressant action of the drug on neurally-evoked transmitter release.

Animals↗
PubMed1995

Calcium-activated release of nitric oxide potentiates excitatory synaptic potentials in immature rat sympathetic preganglionic neurons.

1. Whole cell patch recordings were made from sympathetic preganglionic neurons (SPNs), the majority of which contain brain nitric oxide synthase (bNOS), in transverse spinal cord slices of 12- to 16-day-old rats. 2. Repetitive discharge of SPNs induced by a train of depolarizing current pulses (40 Hz. 10 s) was followed by a long-lasting increase (140 +/- 22%, mean +/- SD) of the amplitude of excitatory postsynaptic potentials (EPSPs) evoked by stimulation of lateral funiculus in 50 of 75 SPNs. 3. In slices pretreated with the nitric oxide synthase inhibitors, NG-monomethyl-L-arginine (L-NMA: 100 microM) or Nw-nitro-L-arginine (L-NARG; 30 microM) or with bovine hemoglobin (100 microM), repetitive discharge of SPNs was not followed by a significant increase of EPSPs. 4. Superfusing the slices with L-arginine (L-Arg, 300 microM) but not D-Arg reversibly increased the EPSPs by an average of 140 +/- 19%. 5. Inclusion of the Ca2+ chelator 1.2-bis(2-aminophenoxy)- ethane-N,N,N',N'-tetraacetic acid (BAPTA, 1 mM) in the patch electrodes resulted in no significant increase of EPSPs after repetitive discharge in all cells studied. 6. It is concluded that during repetitive discharge of SPNs, Ca2+ influx via voltage-gated channels activates bNOS, resulting in a release of nitric oxide and potentiation of EPSPs.

Adrenergic Fibers↗
PubMed1995

The origin of Gaussian distributions of synaptic potentials.

Spontaneous synaptic potentials were identified at the motor endplate 40 years ago. These were shown to possess amplitudes that could be described by a Gaussian distribution as could the amplitudes of evoked synaptic potentials under conditions of very low probability for secretion. As these Gaussians were identical, the idea of a unit or quantum of transmission was conceived. The failure to obtain similar Gaussian distributions for both spontaneous and low-probability evoked potentials during development of endplates indicated that a unit of transmission was not operating. However both the spontaneous and very low-probability evoked potentials could each be described by mixtures of Gaussians indicating a subunit of transmission might be operative. There are no ganglionic or central synapses at which comparisons have been made between spontaneous and low-probability evoked potentials that show each can be described by a Gaussian distribution, let alone that these are the same indicating a unit of transmission as originally conceived. There is some evidence that mixtures of Gaussians can be used to describe both spontaneous and very low-probability evoked synaptic potential amplitudes, opening up the possibility for a subunit of transmission at these synapses. The vesicle hypothesis, that the quantum of transmission at the endplate is due to the exocytosis of the contents of a synaptic vesicle, was also enunciated nearly 40 years ago. The existence of subunits of transmission has required reconsideration of this hypothesis. Three alternatives are considered: in one, the calcium-transient hypothesis, the subunit of secretion is due to the release of calcium from one of several calcium stores in the nerve terminal, so that several subunits are released when a number of these calcium stores are engaged in a regenerative response to the terminal action potential; a second alternative, the mediatophore hypothesis, is that a subunit of secretion occurs when a single transmitter transport protein channels transmitter across the terminal membrane, several such mediatophore proteins acting in concert then give multiple subunit release; finally, there is the vesicle fusion-pore hypothesis, in which individual transient openings of a fusion-pore channel joining a synaptic vesicle to the terminal membrane are responsible for secretion of a transmitter subunit, with multiple transients giving several subunits. Perhaps we will have distinguished between these possibilities before the quantal hypothesis is 50 years old.

Animals↗
PubMed1991

Adenosine (A2) antagonist inhibits induction of long-term potentiation of evoked synaptic potentials but not of the population spike in hippocampal CA1 neurons.

The effects of adenosine A2 receptor antagonist (CP-66713) on long-term potentiation were studied using guinea pig hippocampal slices in a perfusion system. Tetanic stimulation of Schaffer collateral input which was applied during perfusion of CP-66713 (10 microM), did not induce long-term potentiation but rather long-term depression of evoked synaptic potentials (field EPSP), but induced long-term potentiation of the population spike in CA1 neurons. Thus, adenosine derivatives which accumulate in the synaptic cleft during the tetanic stimulation may be involved in induction of the long-term potentiation via A2 receptors at the synapse. The clear discrimination between long-term depression of the field EPSP and long-term potentiation of the population spike suggests EPSP-spike potentiation at the postsynaptic sites.

Animals↗
PubMed1981

Post-tetanic potentiation and facilitation of synaptic potentials evoked in cat spinal motoneurones.

1. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in spinal alpha-motoneurones of the cat by impulses in single group Ia nerve fibres. 2. The average peak amplitude of some of these e.p.s.p.s was increased by a conditioning tetanus. The maximum increase observed was 54% of the control amplitude. 3. The average peak amplitude of some e.p.s.p.s was increased by a single conditioning stimulus which preceded the test stimulus by 1 or 2 msec. The maximum increase observed was 28% of the control amplitude. 4. The ability of e.p.s.p.s to potentiate following a tetanus was correlated with their ability to be facilitated by a single conditioning stimulus. 5. If an e.p.s.p. could be facilitated prior to a tetanus, the amount of facilitation was reduced after the tetanus, with all facilitation being abolished when post-tetanic potentiation was maximal. 6. The fluctuations of an e.p.s.p. were analysed before and after a tetanus. The peak amplitudes that an e.p.s.p. fluctuated between while potentiated did not gradually diminish as the effect of the tetanus disappeared. Post-tetanic potentiation, when it occurred, was accompanied by a decrease in the probability of occurrence of components with smaller peak amplitudes and an increase in the probability of occurrence of components with larger peak amplitudes. 7. These results are consistent with the suggestion that the magnitude of the synaptic potential generated at a single bouton does not vary from trial to trial (Jack, Redman & Wong, 1981a). Nor does the amplitude of this potential vary following a single conditioning stimulus or a tetanus. Post-tetanic potentiation and facilitation result from a decrease in the probability of failure to release transmitter following the conditioning stimuli.

Animals↗
PubMed1998

Brain-derived neurotrophic factor rapidly potentiates synaptic transmission through NMDA, but suppresses it through non-NMDA receptors in rat hippocampal neuron.

Brain-derived neurotrophic factor (BDNF) rapidly enhances synaptic transmission among the hippocampal neurons. In order to examine which component of glutamate receptors participates in synaptic potentiation by BDNF, we have studied the effect of glutamate antagonists on excitatory postsynaptic currents (EPSCs) enhanced by BDNF, using cultured embryonic hippocampal neurons. In the presence of AP5, a N-methyl-D-aspartate (NMDA) antagonist, BDNF depressed the EPSCs. In contrast, BDNF enhanced the EPSCs in the presence of a non-NMDA antagonist CNQX. Our results suggest that BDNF acutely activates synaptic transmission via NMDA, but suppresses it via non-NMDA receptors in the hippocampus.

2-Amino-5-phosphonovalerate↗
PubMed1977

Post-tetanic potentiation, habituation and facilitation of synaptic potentials in reticulospinal neurones of lamprey.

1. Synaptic potentials evoked by electrical stimulation of cranial nerves were recorded in giant reticulospinal neurones (Müller cells) of lamprey. A variety of patterns of stimulation was employed to explore further the functional properties of the pathways intervening between the cranial nerve fibres and Müller cells.2. Simultaneous low intensity stimulation of two different cranial nerves produced excitatory short-latency synaptic potentials whose amplitudes summed linearly.3. Tetanic (10/sec) stimulation of a cranial nerve depressed the evoked short-latency synaptic response, but following the tetanus the synaptic response was potentiated above control amplitude for several minutes. Tetanic stimulation of one cranial nerve had no effect upon the synaptic responses evoked by stimulation of other cranial nerves.4. Low-frequency stimulation (1/sec to 1/20 sec) of a cranial nerve produced a progressive decrease in the amplitude of the evoked short-latency synaptic response. This phenomenon was termed synaptic habituation because its characteristics were functionally similar to behavioural habituation in animals.5. Habituation of the synaptic response to stimulation of one cranial nerve had no effect on the synaptic responses produced by stimulation of other cranial nerves.6. Synaptic afterdischarges lasting from several seconds to several minutes were recorded in Müller cells. They occurred both spontaneously and in response to strong electrical stimulation of cranial nerves. For several minutes following an afterdischarge the amplitudes of short-latency synaptic potentials produced by stimulation of any one of the cranial nerves were increased as much as twofold. This facilitation occurred equally well whether the short-latency synaptic responses had been habituated or not.7. A theoretical cell-wiring diagram is proposed to account for the properties of short-latency evoked synaptic responses and synaptic afterdischarges and for the facilitation of short-latency responses by afterdischarges.

Animals↗
PubMed1958

Synaptic potential in the motor giant axon of the crayfish.

Some electrical properties of the synapses between central giant axons (presynaptic) and the motor giant axon (postsynaptic) of the crayfish abdominal nerve cord have been investigated. Postsynaptic potential change in response to presynaptic volleys contains two components: a spike potential and a synaptic potential of very long time course. Amplitude of the synaptic potential is graded according to the number of active presynaptic axons. Conductance increase in the synaptic membrane endures over most of the period of potential change, and it is this rather than the "electrical time constant" of the membrane that in large measure determines the form of the synaptic potential. Temporal summation of synaptic potential occurs during repetitive presynaptic stimulation, and after such stimulation the rate of decay of synaptic potential is greatly slowed.

Action Potentials↗
PubMed2000

A novel SNAP25-caveolin complex correlates with the onset of persistent synaptic potentiation.

We have identified synaptic protein complexes in intact rat hippocampal slices using the rapid chemical cross-linking reagent paraformaldehyde. Cellular proteins were rapidly cross-linked, solubilized, separated electrophoretically by SDS-PAGE, and then identified immunologically. Multiple complexes containing syntaxin, the synaptosomal-associated protein of 25 kDa (SNAP25), and vesicle-associated membrane protein (VAMP) were observed to coexist in a single hippocampal slice including a 100 kDa cross-linked protein complex that exhibited the same electrophoretic migration as a member of the previously identified SDS-resistant soluble N-ethylmaleimide-sensitive fusion attachment protein receptor "core" of the 20 S complex. A VAMP-synaptophysin complex, reported previously in vitro, was also observed in the hippocampal slices. This study links biochemical and physiological studies involving presynaptic proteins implicated in secretion and confirms that these proteins that have been studied extensively previously in the presence of detergent do form "bona fide" cellular complexes. Importantly, we have also detected additional novel protein complexes that do not correspond to complexes identified previously in vitro. After the induction of persistent synaptic potentiation, an abundant 40 kDa SNAP25-caveolin1 complex was observed. The SNAP25-caveolin1 complex was not abundant in control slices and, therefore, represents the first demonstration of a reorganization of protein complexes in intact hippocampal slices during the induction of synaptic potentiation. The interaction between caveolin1 and SNAP25 was confirmed biochemically by demonstration of the association of caveolin with recombinant-immobilized SNAP25 and by the coimmunoprecipitation of SNAP25 using caveolin-specific antisera. Caveolin1, like SNAP25, was observed to be abundant in isolated hippocampal nerve terminals (synaptosomes). Immunofluorescent studies demonstrated that both SNAP25 and caveolin1 are present in neurons and colocalize in axonal varicosities. These results suggest that a short-lasting SNAP25-caveolin interaction may be involved in the early phase of synaptic potentiation.

Animals↗