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At least 415 records · Page 23Linked to original sources
PubMed1989

ATP-induced synaptic potentiation in hippocampal slices.

The purpose of this study was to investigate the influence of different adenosine triphosphate (ATP) concentrations (ranging from 400 nM to 250 microM) on hippocampal potentials recorded from pyramidal neurons. ATP applied at a concentration of 400 nM induced a 100% increase in the size of the population spike (potentiation). The potential started to increase 30-60 s after ATP application, reached a maximum after 20 min, and remained potentiated for longer than 1.5 h. Washing the slices with fresh Ringer solution did not reverse the effect. ATP applied at a concentration of 50-150 microM, temporarily depressed the potential. This depression, however, was transient, as the potential gradually recovered by itself and reached a value higher than that observed before ATP application. ATP applied at the concentration of 250 microM caused a long-lasting depression of the potential. The potential was not restored by washing the slices, but recovered after addition of 0.7 microM 3,4-diaminopyridine. These data show a concentration-dependent mode of ATP action on hippocampal neurons and suggest a role for ATP in regulating synaptic efficiency.

Action Potentials↗
PubMed1995

Effects of losigamone on synaptic potentials and spike frequency habituation in rat entorhinal cortex and hippocampal CA1 neurones.

Losigamone is an anticonvulsant both in vivo and in vitro. We here studied possible mechanisms for such effects with conventional intracellular recordings from pyramidal cells of area CA1 and entorhinal cortex in combined hippocampal-entorhinal cortex slices. Losigamone reversibly reduced the number of action potentials elicited by 1 s long depolarising current injections. In addition, the drug moderately reduced EPSP amplitudes while monosynaptic fast and slow IPSPs were unaffected.

Action Potentials↗
PubMed1976

[Synaptic potentials in smooth muscle cells].

Investigations were carried out on smooth muscle cells (SMC) of rat and rabbit anococcygeus by the method of a double "sugar bridge" in the presence of tetraethylammonium (1 mM/1) in the Krebs solution. Stimulation of the muscle strip by the electric current rectangular pulse of the maximal value and of short duration caused the development of excitatory postsynaptic potentials (EP SP) in the rat and rabbit SMC, and of inhibitory postsynaptic potentials in the rabbit SMC. The value of postsynaptic potentials displayed a linear dependence on the level of the membrane potential. Elimination of chlorine ions from the external solution decreased the EP SP of the SMC of rabbit anococcygeus and shifted the reversion potential in the direction of sodium balance potential. Apparently generation of the EP SP of the SMC of rabbit anococcygeus was associated with the increased permeability of the membrane both for sodium and for chlorine ions.

Action Potentials↗
PubMed1986

Low frequency perforant path stimulation as a conditioned stimulus demonstrates correlations between long-term synaptic potentiation and learning.

Stimulation of the perforant path with impulse trains of 15 cps and 670 msec duration was used as a conditioned stimulus in a two-way shuttle box avoidance on rats. Field potentials in the dentate area evoked by test stimuli were measured after the training sessions until the 7th day. Foot-shock and unconditioned escape elicited only a transient slight depression of the population spike amplitude (P) and increased also slightly the slope function (SF) of the population EPSP of the evoked test potentials. The control stimulation of the perforant path without pairing with foot-shock as in conditioning did only slightly increase SF of test potentials, but produced a strong transient inhibition followed by a long lasting moderate depression of P. After conditioning, all animals exhibited the same initial inhibition of P as shown in control stimulation of the perforant path. However during the following 4 hours, good learners with a relearning index greater than 30% developed a significant potentiation of P lasting until the second training session 24 hours later, which resulted in a further enhancement. SF of the evoked test potentials increased in good learners with a similar time course after conditioning but without initial depression. After 7 days P showed still enhanced but non-significant values. Poor learners with a relearning index less than 10% did not develop a potentiation of P after conditioning and initial inhibition, but a long-term depression. Also SF of test potentials decreased in poor learners during 4 hours after conditioning and returned almost to baseline until the following day. After 7 days, P and SF did not differ from baseline. The analysis of the observed synaptic changes by E-S curves demonstrated the post-tetanic LTP seems to differ in some ways from post-conditioning LTP in good learners. The latter exhibits a clear tendency of a right shift contrary to the left shift commonly occurring after tetanization. Furthermore poor learners do not only fail to produce long-term potentiation, but fail to show a change in the opposite direction with a left shift of the E-S curves. The observed correlation of LTP in the conditioning pathway with the learning ability suggests an involvement of LTP at least in the acquisition and early retention of this learned behavior. The results do however not finally clarify the role of LTP in long-term retention.

Animals↗
PubMed1993

Effects of temperature on synaptic potentials in the locust flight system.

1. Neuronal circuitry in the locust flight system operates normally within a temperature range of 24-42 degrees C. I investigated the effects of temperature on parameters of postsynaptic potentials generated in different neurons following action potentials of the forewing stretch receptor. 2. Increases in temperature reduced latency, time-to-peak and duration (Q10s = 0.51, 0.70, and 0.68, respectively; 24-34 degrees C) and increased the slope (Q10 = 1.13; 24-34 degrees) of the excitatory postsynaptic potential (EPSP). However, increases in temperature increased EPSP amplitude below room temperature (Q10 = 1.25; 14-24 degrees C) but decreased EPSP amplitude above room temperature (Q10 = 0.80; 24-34 degrees C). 3. I conclude that neuronal and synaptic function were affected by temperature in ways predictable by well-established thermal effects on channel conductance and kinetics and on membrane properties. Thus temperature compensation of the output of the flight system must be mediated in some way by the operation of the circuitry. 4. I propose that below room temperature EPSP amplitude was increased by predominant effects on channel conductance and membrane time constant, and above room temperature EPSP amplitude was decreased by a predominant effect on the amplitude and duration of the presynaptic action potential. Further, I suggest that the frequency of the output rhythm is unaffected by the amplitude of single EPSPs, within permissive limits.

Animals↗
PubMed1984

[Antidromic and synaptic potentials of neurons of the lateral vestibular nucleus of the cat evoked by stimulation of the interstitial nucleus of Cajal and the nucleus of Darkschewitsch].

Effects of stimulation of the Cajal interstitial nucleus and Darkschewitsch nucleus on the activity of neurons of the lateral vestibular nucleus of Deiters was studied in experiments on cats anesthetized with nembutal. It was shown that stimulation of the mentioned structures lead to antidromic and synaptic activation of Deiters neurons. Ascending axon collaterals of vestibular neurons to the marked brain stem structures were revealed. Stimulation of both Cajal and Darkschewitsch nuclei evoked mono- and polysynaptic EPSP and IPSP in Deiters neurons. The convergence of influences from both nuclei on the investigated neurons was shown. Peculiarities and functional significance of the indicated influences are discussed.

Animals↗
PubMed1995

Synaptic potentials and threshold currents underlying spike production in motor giant axons of Aglantha digitale.

1. Motor giant axons that excite swimming muscles in the jelly-fish Aglantha digitale interface with units of the inner and outer nerve rings in the margin at the base of the bell. External recording electrodes were used to monitor electrical activity at different sites within the nerve ring while events in the motor giant axon were recorded with intracellular micropipettes placed within 100 microns of the synaptic area. In some experiments, 4- to 6-micron-diam patch pipettes were used to record in situ from ion channel clusters at different locations along the axon. 2. Independently propagating calcium and sodium spikes in the motor giant axon were found to arise from different excitatory postsynaptic potentials (EPSPs). Two separate inputs were identified; one EPSP class represented an input from the pacemaker system in the inner nerve ring, whereas another represented an input from the giant axon in the outer nerve ring. EPSPs from the two nerve rings had significantly different time courses and amplitudes. EPSPs from the ring giant axon reached a peak in little more than 1 ms, whereas EPSPs from the pacemaker system reached a maximum in approximately 7 ms. These slower EPSPs may be compound events composed of postsynaptic potentials from multiple synapses excited in series by the passage of the pacemaker neuron signal. 3. The threshold for the production of calcium spikes by the slow EPSPs of the pacemaker system (-51 +/- 2.2 mV, mean +/- SD; n = 5) corresponded well with the voltage at which a net inward "T"-type calcium current first appeared in recordings from axon membrane patches (-55 to -50 mV); the threshold for the initiation of the sodium spike by the fast EPSPs of the ring giant system (-32 +/- 1.2 mV, mean +/- SD; n = 6) corresponded well with the voltage at which a net inward sodium current first appeared (-35 to -30 mV). 4. Inward currents were rarely observed in membrane patches formed using pipettes with tips of < 1 micron OD. Even with 4-micron pipettes, patches of membrane were sometimes obtained with a channel population consisting exclusively of potassium channels; calcium and sodium currents were found in highly discrete areas ("hot spots"). Preliminary findings on the undersurface of the axon, which makes synaptic contact with the myoepithelium, are consistent with a similar distribution. 5. The pathway by which the ring giant excites the motor giant axon is not definitely known. The synaptic delay between the peak of the ring giant action potential (monitored externally) and the initial rise of the fast EPSP (1.64 +/- 0.15 ms, mean +/- SD; n = 21) would allow for transmission at two synapses, because single synaptic delays at neuromuscular junctions in Aglantha are approximately 0.7 ms at 12 degrees C. The mean synaptic delay at the slow EPSP synapse was 0.88 +/- 0.09 (SD) ms (n = 12). 6. The delay between the impulse in the ring giant axon and the subsequent excitation of the motor giant axon may permit the animal to withdraw its tentacles and so lower the drag that would otherwise reduce the effectiveness of any escape swim and might induce tentacle autotomy.

Action Potentials↗
PubMed2006

Altered hippocampal synaptic potentiation in P2X4 knock-out mice.

P2X4 purinergic receptors are calcium-permeable, ATP-activated ion channels. In the CA1 area of the hippocampus, they are located at the subsynaptic membrane somewhat peripherally to AMPA receptors. The possible role of P2X4 receptors has been difficult to elucidate because of the lack of selective antagonists. Here we report the generation of a P2X4 receptor knock-out mouse and show that long-term potentiation (LTP) at Schaffer collateral synapses is reduced relative to that in wild-type mice. Ivermectin, which selectively potentiates currents at P2X4, was found to increase LTP in wild-type mice but had no effect in P2X4 knock-out mice. We suggest that calcium entry through subsynaptic P2X4 receptors during high-frequency stimulation contributes to synaptic strengthening.

Animals↗
PubMed1983

[Analysis of polymodality in the distribution of latent periods and amplitudes of single-quantum synaptic potentials in the frog neuromuscular junction].

Intracellular recording with low concentrations of Ca2+ ions as analysed in the histograms of latency values and amplitude distributions, revealed 4-7 peaks in unitary potentials from the neuromuscular junction in the frog sartorius muscle. The increase of Ca2+ ions concentration led to disappearance of the multimodality. Extracellular recording revealed but a single mode in histograms of distributions. The number of modes in latency values distributions was found to have a positive correlation with values of the binominal parameter n and the number of peaks in histograms of the EP amplitudes. The peaks in histograms of distribution of the latency values and amplitudes of unitary EPs seem to reflect the action of transmitter release in the nerve terminals.

Action Potentials↗
PubMed2000

Theoretical analysis of the amplification of synaptic potentials by small clusters of persistent sodium channels in dendrites.

We extend on the work developed by R.R. Poznanski and J. Bell from a linearized somatic persistent sodium current source to a non-linear representation of the dendritic Na(+)P current source associated with a small number of persistent sodium channels. The main objective is to investigate the modulation in the amplification of excitatory postsynaptic potentials (EPSPs) in dendrites studded with persistent sodium channels. The relation between membrane potential (V) and persistent sodium current density (I(NaP)) is approximated heuristically with a sigmoidal function and the resultant cable equation is solved analytically using a regular perturbation expansion and Green's function techniques. The transient simulated (non-evoked) response is found as a result of current injection in the form of synaptically induced voltage change located at a distance from the recording site in a cable with a uniform distribution of ion channel densities per unit length of cable (the so-called 'hot-spots') and with the conductance of each hot-spot (i.e., number of channels per hot-spot) assumed to be a constant. The results show an amplification in the observed EPSPs to be compatible with the experimentally derived estimates, and in addition a saturation in the amplification is observed indicating an optimum number of ionic channels.

Animals↗
PubMed1997

Muscarinic reduction of GABAergic synaptic potentials results in disinhibition of the AMPA/kainate-mediated EPSP in auditory cortex.

The present study is concerned with the ability of muscarinic actions of acetylcholine (ACh) to modulate glutamate and gamma-aminobutyric acid (GABA)-mediated synaptic transmission in the in vitro rat auditory cortex. Whole-cell patch clamp recordings were obtained from layer II-III pyramidal neurons, and the fast-EPSP (AMPA/kainate), fast-IPSP (GABA(A)), and slow-IPSP (GABA(B)), were elicited following a stimulus to deep gray/white matter. Acetyl-beta-methylcholine (MCh), a muscarinic receptor agonist, applied by either superfusion or iontophoresis, produced an atropine-sensitive increase or decrease in the amplitude of the fast-EPSP. The effect of MCh could be predicted by the response of the fast-EPSP to paired-pulse stimulation (i.e. a conditioning pulse followed 300 ms later by a test pulse). The fast-EPSP was decreased in amplitude by MCh in cases where the test-EPSP was suppressed in the pre-MCh condition, and increased in amplitude when the test-EPSP was facilitated. The fast- and slow-IPSPs were always reduced by MCh. In several experiments, the strength of synaptic inhibition was systematically modified by varying stimulus intensity. When the fast-EPSP was elicited in the absence of IPSPs, it was decreased in amplitude by MCh. However, when the fast-EPSP was elicited in conjunction with large IPSPs it was increased in amplitude during MCh. Because the magnitude of the fast-EPSP is influenced by the degree of temporal overlap with IPSPs, it was hypothesized that enhancement of the fast-EPSP was the result of disinhibition produced as a consequence of muscarinic reduction of GABAergic IPSPs. This view was supported by the finding that MCh could reduce the amplitude of pharmacologically isolated GABAergic IPSPs (i.e. elicited in the absence of glutamatergic transmission). Our results suggest that ACh at muscarinic receptors can modify fast glutamatergic neurotransmission differently as a function of strength of inhibition, to suppress that produced by 'weak' inputs and enhance that produced by 'strong' inputs.

Acetylcholine↗
PubMed2000

A dendritic cable model for the amplification of synaptic potentials by an ensemble average of persistent sodium channels.

The persistent sodium current density (I(NaP)) at the soma measured with the 'whole-cell' patch-clamp recording method is linearized about the resting state and used as a current source along the dendritic cable (depicting the spatial distribution of voltage-dependent persistent sodium ionic channels). This procedure allows time-dependent analytical solutions to be obtained for the membrane depolarization. Computer simulated response to a dendritic current injection in the form of synaptically-induced voltage change located at a distance from the recording site in a cable with unequally distributed persistent sodium ion channel densities per unit length of cable (the so-called 'hot-spots') is used to obtain conclusions on the density and distribution of persistent sodium ion channels. It is shown that the excitatory postsynaptic potentials (EPSPs) are amplified if hot-spots of persistent sodium ion channels are spatially distributed along the dendritic cable, with the local density of I(NaP) with respect to the recording site shown to specifically increase the peak amplitude of the EPSP for a proximally placed synaptic input, while the spatial distribution of I(NaP) serves to broaden the time course of the amplified EPSP. However, in the case of a distally positioned synaptic input, both local and nonlocal densities yield an approximately identical enhancement of EPSPs in contradiction to the computer simulations performed by Lipowsky et al. [J. Neurophysiol. 76 (1996) 2181]. The results indicate that persistent sodium channels produce EPSP amplification even when their distribution is relatively sparse (i.e. , approximately 1-2% of the transient sodium channels are found in dendrites of CA1 hippocampal pyramidal neurons). This gives a strong impetus for the use of the theory as a novel approach in the investigation of synaptic integration of signals in active dendrites represented as ionic cables.

Animals↗