Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Synaptic Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1997

Brain-derived neurotrophic factor and nerve growth factor potentiate excitatory synaptic transmission in the rat visual cortex.

1. The effect of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) on excitatory synaptic transmission in the developing visual cortex was studied by whole-cell patch-clamp recordings from rat brain slices. 2. Both neurotrophins induced a rapid increase in the amplitude of impulse-evoked excitatory postsynaptic currents (EPSCs). BDNF also increased the frequency of spontaneous EPSCs. 3. Analysis of the currents revealed that alpha-amino-3-hydroxy-5-methyl-isoxazole propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components contributing to the EPSC peak amplitude were equally potentiated by the neurotrophins. 4. When synaptic transmission was studied by minimal stimulation of intracortical afferents, neurotrophins induced a decrease in the occurrence of release failures. 5. A number of neurones were insensitive to the effects of the neurotrophins, possibly related to the considerable heterogeneity of neuronal types and to the uneven distribution of neurotrophin receptors in the visual cortex. 6. The probability of neurotransmitter release represents a rapidly modifiable synaptic feature by which neurotrophins can potentiate the efficacy of excitatory synaptic transmission in the visual cortex.

Animals↗
PubMed1990

Cyclic adenosine monophosphate (cAMP)-induced potentiation of synaptic responses in Helix neurons.

1. The effect of intracellularly injected cAMP on the amplitude of excitatory postsynaptic potentials was studied using identified neurons of the snail Helix pomatia. 2. In 25% of the experiments, postsynaptic cAMP elevation caused a pronounced augmentation of the excitatory postsynaptic potential (EPSP) amplitude, lasting up to 15-30 min. 3. The results suggest that a cAMP increase in the postsynaptic neuron may be involved in the enhancement of synaptic efficiency.

Action Potentials↗
PubMed1987

Long-lasting potentiation of synaptic transmission requires postsynaptic modifications in the neocortex.

The mechanisms of associative long-lasting potentiation (LLP) of excitatory postsynaptic potentials (EPSPs) were studied in the motor cortex of anesthetized cats. Mono- and oligosynaptic EPSPs were evoked by stimulations of thalamic VL nucleus, pyramidal tract, callosal and somatosensory system and paired with orthodromic, antidromic or current-induced action potentials. EPSP-spike stimulus pairs with 0.1-0.2 Hz frequency and 0-200 ms interstimulus intervals induced increases in the amplitudes and durations of EPSPs for 40-60 min or longer after 20-50 pairings. The LLP was prevented when postsynaptic firing was blocked by intracellular current injection or by juxtasomatic application of gamma-aminobutyric acid. LLP was also prevented when the level of intracellular free calcium was lowered by the intracellular injection of the calcium chelator EGTA or when neuronal transport was blocked by the intracellular injection of colchicine. Neither EGTA nor colchicine blocked postsynaptic firing. Thus, these findings show that LLP in the neocortex is a postsynaptic phenomenon which requires conjunctive pre- and postsynaptic activity, adequate levels of intracellular free calcium, and functional intracellular transport.

Action Potentials↗
PubMed1971

Influence of the latency fluctuations and the quantal process of transmitter release on the end-plate potentials' amplitude distribution.

Spontaneous synaptic potentials and their relation to the end-plate potential (e.p.p.) are studied. It has been suggested earlier that the e.p.p. at a single nerve-muscle junction is built up statistically of small all-or-none units which are identical in size with the spontaneous miniature end-plate potentials (m.e.p.p.'s). In this paper, a more general theory is developed which takes into account latency fluctuations of the unit components. A general equation for e.p.p. amplitude probability distribution is derived. This probability distribution is a function of the latency distribution, m.e.p.p.'s pulse shape, m.e.p.p.'s amplitude distribution, and the mean quantal content. The time course of transmitter release, or latency distribution, is derived from a histogram of synaptic delays in a frog muscle, but obtained equations can be used for other distribution functions as well.

Computers↗
PubMedDate not supplied

Long-term potentiation induces synaptic plasticity at nontetanized adjacent synapses.

The two forms of long-term potentiation (LTP) and one form of long-term depression (LTD) in hippocampal area CA1 are induced by different afferent tetani: LTD is induced by a 3- to 5-Hz tetanus, whereas higher frequencies are necessary for LTP mediated by NMDA receptors (25- to 50-Hz tetanus) and LTP mediated by voltage-dependent calcium channels (200-Hz tetanus). It has been suggested that the three forms are induced by graded increases in postsynaptic calcium, with LTD being induced at the lowest calcium concentration. We hypothesized that synapses near a site of LTP induction would elicit LTD owing to diffusion of calcium or its binding proteins. This was tested using a fixed multistimulating electrode array spanning stratum radiatum in area CA1 of rat hippocampal slices. The tetanized sites all displayed LTP. Nontetanized sites displayed LTD following a 50-Hz tetanus, whereas LTD was often seen following a 200-Hz tetanus. In most instances pEPSP and population spike responses were similar; however, EPSP/spike dissociations (LTD of EPSP, LTP of spike) were seen following activation of NMDA receptors by 50-Hz and 200-Hz tetani. The results are discussed with respect to mechanisms of action and functional significance.

Action Potentials↗
PubMed2005

Effects of the mGluR8 agonist (S)-3,4-DCPG in the lateral amygdala on acquisition/expression of fear-potentiated startle, synaptic transmission, and plasticity.

The lateral amygdala plays an important role in emotional learning. Previous studies found that amygdaloid plasticity processes involve the activation of metabotropic glutamate receptors. In the present study we examined the effect of the highly specific mGluR8 agonist (S)-3,4-DCPG on conditioned fear in vivo measuring fear-potentiated startle. Both, acquisition and expression of conditioned fear were dose-dependently inhibited by (S)-3,4-DCPG injections into the amygdala. Since synaptic long-term potentiation in the lateral amygdala has been correlated with the acquisition of conditioned fear in rats, the effect of (S)-3,4-DCPG in vitro on synaptic transmission, short- and long-term plasticity in the lateral amygdala was evaluated in parallel. Patch clamp recordings in rat brain slices revealed that (S)-3,4-DCPG strongly attenuated synaptic transmission from sensory afferents. The lack of detectable effects on postsynaptic neurons and altered short-term plasticity indicate that (S)-3,4-DCPG acts at presynaptic sites. Long-term potentiation of thalamic afferent fiber synapses induced by a pairing protocol was slightly attenuated in the presence of (S)-3,4-DCPG, but long-term potentiation by tetanic afferent stimulation was inhibited. We conclude that mGluR8 activation is not specifically involved in long-term plasticity processes but that it rather provides a powerful inhibitory control of synaptic transmission within the lateral amygdala, with the ability to reduce activity in such a way that the expression and the acquisition of learned fear become strongly impaired in vivo.

Amygdala↗
PubMed1987

Intrinsic features contributing to spike train patterning in proprioceptive cuneate neurons.

The intrinsic processes contributing to the three discharge patterns of proprioceptive cuneate neurons described by Surmeier and Towe were studied experimentally and with computer simulation. Examination of the alterations in excitability produced by antidromic activation suggested that a prolonged inhibition was a concomitant of discharge in proprioceptive cuneate neurons. Computer simulation was performed to test the possible roles of inhibitory hyperpolarizing processes in governing the observed discharge patterns. These simulations used two constant threshold models. The simplest model linearly integrated synaptic potentials until the spike threshold was reached. After the discharge, synaptic potentials that preceded the spike were ignored (i.e., the model was "reset"). The second model was similar to the first except that following a spike two hyperpolarizing processes were activated and preceding events continued to play a role in membrane potential. Simulation of class A spike trains that possessed positive correlations between nearby intervals was successful only with a resetting model. This suggested that class A neurons have fast, no-memory postspike conductance changes, which effectively shunt synaptic charge. Simulation of class B spike trains was possible with the nonresetting model. At least two periodic inputs, which evoked brief, relatively large EPSPs, were required. In addition, a prominent, fast, spike-dependent hyperpolarization and a small-amplitude, slow hyperpolarization were required. Simulation of class C spike trains was also possible with the nonresetting model. Several periodic inputs were required; one input had to evoke a slow suprathreshold EPSP. In contrast to class B simulations, class C spike train simulation required that a large-amplitude, slow hyperpolarization, as well as a brief hyperpolarization, following spike initiation. The results of class B and C simulations suggested that these two groups differed primarily in the amplitude of a slow, hyperpolarizing, postspike conductance. Some role may also be played by the time course of the driving EPSPs.

Animals↗
PubMed2004

Multiple forms of long-term potentiation and long-term depression converge on a single interneuron in the leech CNS.

Long-term potentiation (LTP) of synaptic transmission was observed in two types of synapses that converge on the same postsynaptic neuron in the leech CNS. These synapses were made by identifiable sensory neurons, the mechanosensory touch (T-) and pressure (P-) cells, onto the S-cell, an interneuron critical for certain forms of learning. Changes in both the T-S and P-S synapses appear to be activity dependent because LTP was restricted to inputs that had undergone tetanization; however, properties of synaptic plasticity at the T-S and P-S connections differ considerably. At the P-S synapse, LTP was induced in the tetanized synapse but not in the nontetanized synapse tested in parallel. P-S LTP was blocked by the NMDA receptor antagonist dl-2-amino-5-phosphono-valeric acid (AP-5) or by lowering the extracellular concentration of glycine, an NMDA receptor (NMDAR) co-agonist. P-S LTP was strongly affected by the initial amplitude of the synaptic potential at the time LTP was induced. Smaller amplitude synapses (<3.5 mV) underwent robust potentiation, whereas the less common, larger amplitude synapse (>3.5 mV) depressed after tetanization. At the T-S synapse, tetanization simultaneously induced homosynaptic LTP in the tetanized input and heterosynaptic long-term depression (LTD) in the input made by a nontetanized T-cell onto the same S-cell. Interestingly, AP-5 failed to block homosynaptic LTP at the T-S synapse but did prevent heterosynaptic LTD. T-S LTP was not affected by the initial EPSP amplitude. Thus, leech neurons exhibit synaptic plasticity with properties similar to LTP and LTD found in the vertebrate nervous system.

Animals↗
PubMed2000

Intracellular Ca(2+) and Ca(2+)/calmodulin-dependent kinase II mediate acute potentiation of neurotransmitter release by neurotrophin-3.

Neurotrophins have been shown to acutely modulate synaptic transmission in a variety of systems, but the underlying signaling mechanisms remain unclear. Here we provide evidence for an unusual mechanism that mediates synaptic potentiation at the neuromuscular junction (NMJ) induced by neurotrophin-3 (NT3), using Xenopus nerve-muscle co-culture. Unlike brain-derived neurotrophic factor (BDNF), which requires Ca(2+) influx for its acute effect, NT3 rapidly enhances spontaneous transmitter release at the developing NMJ even when Ca(2+) influx is completely blocked, suggesting that the NT3 effect is independent of extracellular Ca(2+). Depletion of intracellular Ca(2+) stores, or blockade of inositol 1, 4, 5-trisphosphate (IP3) or ryanodine receptors, prevents the NT3-induced synaptic potentiation. Blockade of IP3 receptors can not prevent BDNF-induced potentiation, suggesting that BDNF and NT3 use different mechanisms to potentiate transmitter release. Inhibition of Ca(2+)/calmodulin-dependent kinase II (CaMKII) completely blocks the acute effect of NT3. Furthermore, the NT3-induced potentiation requires a continuous activation of CaMKII, because application of the CaMKII inhibitor KN62 reverses the previously established NT3 effect. Thus, NT3 potentiates neurotransmitter secretion by stimulating Ca(2+) release from intracellular stores through IP3 and/or ryanodine receptors, leading to an activation of CaMKII.

Animals↗
PubMed1996

Synaptic modulation by neurotrophic factors: differential and synergistic effects of brain-derived neurotrophic factor and ciliary neurotrophic factor.

Extracellular application of brain-derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF) to developing neuromuscular junctions in Xenopus nerve-muscle cultures resulted in an increase in the frequency of spontaneous synaptic currents (SSCs) and in the amplitude of nerve-evoked synaptic currents. Analyses of the amplitude and time course of the SSCs suggest that these effects are attributable to elevation of presynaptic transmitter release. The actions of these two factors on the transmitter secretion process, however, are distinctly different. Fura-2 Ca2+ imaging showed that an increase in presynaptic cytosolic Ca2+ ([Ca2+]i) accompanied the synaptic potentiation by BDNF, whereas no change in [Ca2+]i was observed during synaptic potentiation by CNTF. Removing external Ca2+ also abolished the potentiating effect of BDNF but did not influence the CNTF effect. Moreover, the two factors exerted different effects on the short-term synaptic plasticity. Paired-pulse facilitation normally found at these synapses was reduced by BDNF but unaffected by CNTF; CNTF, but not BDNF, reduced the extent of synaptic depression during high-frequency tetanic stimulation. Finally, the potentiation effect of BDNF and CNTF on spontaneous transmitter release was additive when both factors were applied together to the synapse at saturating concentrations (100 ng/ml) and was highly synergistic when low doses (1 and 10 ng/ml) of both factors were used. These results suggest that because of their differential effects on the secretory machinery, BDNF and CNTF may act cooperatively in modulating the development and functioning of synapses.

Animals↗
PubMed1983

Evidence for taurine as an inhibitory neurotransmitter in cerebellar stellate interneurons: selective antagonism by TAG (6-aminomethyl-3-methyl-4H,1,2,4-benzothiadiazine-1,1-dioxide).

Using a novel amino acid antagonist, TAG (6-aminomethyl-3-methyl-4H,1,2,4-benzothiadiazine-1,1-dioxide), intradendritic electrophysiological investigations were carried out to obtain evidence for taurine as a neurotransmitter in the cerebellum. The hyperpolarizing action of taurine on Purkinje cell dendrites in guinea pig cerebellar slices was selectively antagonized by TAG (200 microM), while the actions of GABA, glycine and beta-alanine were virtually unaffected. TAG shifted the log dose-response curve of the taurine action to the right in parallel, indicating a competitive antagonism. A hyperpolarizing synaptic potential which was evoked by electrical stimulation of the upper region of the cerebellar molecular layer and recorded from a Purkinje cell dendrite, was reversed to a depolarizing one at a membrane potential of -70 mV. The hyperpolarization induced by exogenously applied taurine was also reversed at the same potential. Moreover, TAG (200 microM) completely and reversibly blocked the synaptic potential. These results suggest that taurine may be an inhibitory neurotransmitter in stellate neuronal synapses on Purkinje cell dendrites.

Animals↗
PubMed1992

Homosynaptic long-term depression in area CA1 of hippocampus and effects of N-methyl-D-aspartate receptor blockade.

We tested a theoretical prediction that patterns of excitatory input activity that consistently fail to activate target neurons sufficiently to induce synaptic potentiation will instead cause a specific synaptic depression. To realize this situation experimentally, the Schaffer collateral projection to area CA1 in rat hippocampal slices was stimulated electrically at frequencies ranging from 0.5 to 50 Hz. Nine hundred pulses at 1-3 Hz consistently yielded a depression of the CA1 population excitatory postsynaptic potential that persisted without signs of recovery for greater than 1 hr after cessation of the conditioning stimulation. This long-term depression was specific to the conditioned input, ruling out generalized changes in postsynaptic responsiveness or excitability. Three lines of evidence suggest that this effect is accounted for by a modification of synaptic effectiveness rather than damage to or fatigue of the stimulated inputs. First, the effect was dependent on the stimulation frequency; 900 pulses at 10 Hz caused no lasting change, and at 50 Hz a synaptic potentiation was usually observed. Second, the depressed synapses continued to support long-term potentiation in response to a high-frequency tetanus. Third, the effects of conditioning stimulation could be prevented by application of NMDA receptor antagonists. Thus, our data suggest that synaptic depression can be triggered by prolonged NMDA receptor activation that is below the threshold for inducing synaptic potentiation. We propose that this mechanism is important for the modifications of hippocampal response properties that underlie some forms of learning and memory.

2-Amino-5-phosphonovalerate↗
PubMed1994

A simulation of action potentials in synaptic boutons during presynaptic inhibition.

1. During presynaptic inhibition, an increased conductance in the membrane of the presynaptic bouton is presumed to reduce the action potential, thereby reducing transmitter release. The object of the simulation has been to determine the magnitude of a chloride conductance required to reduce transmitter release, for various diameters of synaptic boutons, connected to axons with diameters in the range 0.1-1.0 microns. 2. A propagating action potential was simulated in axons connected to either side of a hemispherical bouton. The axons could be myelinated or unmyelinated, while the bouton membrane could be passive, a node of the myelinated nerve, or have the same active properties as the attached unmyelinated nerve. Membrane properties of the axons were derived from mammalian data and scaled to 37 degrees C. 3. A steady-state chloride conductance was included in the bouton membrane, with ECl = -40 mV. The amplitude of the action potential in the bouton was calculated for different diameters of axon and bouton and for different magnitudes of chloride conductance. 4. Using published data on the relationship between the amplitude of a presynaptic action potential and the resulting postsynaptic potential, the relationship between the chloride conductance and the postsynaptic response was calculated for different geometries. Transmitter release was reduced when an action potential was 90 mV or smaller, with no transmission for action potentials smaller than 50 mV. 5. Conductance increases in the range 3 to 10 nS were required to reduce the action potential to 90 mV, depending on the diameter of the axon (0.5-1.0 microns), diameter of the bouton (3-6 microns), whether the bouton had passive or active membrane, and whether the axon was myelinated or unmyelinated. A 3 microns passive bouton connected to a 0.5 micron myelinated axon was most sensitive to the effects of a chloride conductance, while a 6 microns active bouton connected to a 1 micron myelinated nerve was least sensitive to the effects of a chloride conductance. 6. The reduction in the action potential was compared when ECl = -40 mV and when ECl = E(rest) = -80 mV. Inactivation of the sodium conductance by terminal depolarization was the dominant influence on the amplitude of the action potential. 7. Conductances that were sufficient to completely block synaptic transmission at a bouton were insufficient to prevent the spread of the action potential away from that bouton.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1991

Co-cultures of inferior olive and cerebellum: electrophysiological evidence for multiple innervation of Purkinje cells by olivary axons.

Slices of inferior olive (IO) and cerebellum were co-cultured for several weeks by means of the roller tube technique. Recordings were carried out intracellularly from Purkinje cells (PCs) which were identified morphologically by intracellular injection of the fluorescent dye Lucifer yellow, or by immunohistochemical stainings with antibodies raised against the 28 kD Ca(2+)-binding protein calbindin. Following stimulation of olivary tissue, an all-or-none full complex spike response was recorded in some PCs consisting of a fast rising spike followed by a depolarizing potential. In other PCs, graded stimulation of the olivary explant induced synaptic potentials which were characterized by step-wise variation in their amplitude and resembled the ones occurring spontaneously. In contrast, only smoothly graded synaptic potentials were observed in cerebellar mono-cultures. These results indicate that some of the PCs in olivo-cerebellar co-cultures are innervated by several olivary neurons.

Action Potentials↗
PubMed2002

Serotonin alters multi-segmental convergence patterns in spinal cord deep dorsal horn and intermediate laminae neurons in an in vitro young rat preparation.

Each spinal neuron has a receptive field that corresponds to stimulation of a specific area of skin or subcutaneous tissue. Receptive fields are plastic and can be altered during development and injury but the actions of neuromodulators, such as serotonin (5-hydroxytryptamine, 5-HT) on receptive field properties are not well known. We used stimulation of multiple adjacent dorsal root spinal segments as a measure of "receptive field size" to determine the effects of 5-HT on multi-segmental convergent input onto neurons in laminae IV-VII. Whole-cell patch-clamp recordings were undertaken in the in vitro hemisected thoracolumbar spinal cord of rats aged 8-10 days old. Based on synaptic responses, neurons could be divided into two predominant groups and 5-HT exerted different effects on these groups. The first group received excitatory post-synaptic potentials (EPSPs) from the homonymous dorsal root but inhibitory post-synaptic potentials (IPSPs) with increasing amplitude from more distant dorsal roots. In this group, 5-HT preferentially depressed the IPSPs from adjacent nerve roots while leaving the EPSP intact. The second group received short-latency EPSPs from all segments stimulated and 5-HT potently depressed all synaptic input. In both populations the depressant actions of 5-HT increased with dose (0.1-10.0 microM). Bicuculline and strychnine did not affect the 5-HT induced short-latency synaptic depression. These results suggest that descending serotonergic systems depress spinal sensory convergence in a graded and differentiated manner. The findings are discussed in relation to the modulation of nociceptive signaling.

Animals↗
PubMed1985

Presynaptic actions of cholinergic agents upon the hair cell-afferent fiber synapse in the vestibular labyrinth of the frog.

Spontaneous activity of semicircular canal afferents in the isolated labyrinth of the frog is altered by bath application of cholinergic agonists. Muscarinic agonists can produce an increase in action potential frequency of individual afferents. This increase develops slowly and is prolonged in the time course of its action. Nicotinic agonists can either increase (most cases) or decrease afferent activity. These effects occur rapidly and decay during the period of activation, suggesting desensitization. Muscarinic effects are blocked by prior administration of atropine and nicotinic effects (both increases and decreases in action potential frequency) by curare. Intracellular recordings reveal that the nicotinic effects on afferent action potential frequency are the result of alterations in the frequency of spontaneous synaptic potentials, indicating a presynaptic site of action on the hair cells for these compounds. This conclusion is supported by the fact that in the presence of high Mg2+/low Ca2+, which blocks hair cell release of transmitter, cholinergic agonists do not affect the resting membrane potential of the vestibular afferent. Electrical stimulation of the VIIIth cranial nerve can result in either an increase or a decrease in spontaneous synaptic potential and action potential frequency of an afferent. These effects are blocked by prior administration of curare or of nicotinic agonists. Repetitive or continuous stimulation of the VIIIth nerve results in a reversible reduction of the evoked response, suggesting desensitization. Transection of the VIIIth cranial nerve two weeks prior to recording eliminates these actions of electrical stimulation, but not the responses to cholinergic agonists, indicating that the effects of electrical stimulation are mediated by centrally arising efferents. These findings confirm that acetylcholine is probably the transmitter released from centrally arising vestibular efferents, and, in addition, demonstrate that efferent-mediated effects are predominantly expressed through nicotinic receptors. Studies comparing the effects of isolation of the semicircular canal alone versus the intact labyrinth suggest that the method of isolation may be an important factor in determining whether efferent activity results in a predominant increase or decrease in afferent activity.

Acetylcholine↗
PubMed1992

Opioids excite dopamine neurons by hyperpolarization of local interneurons.

Increased activity of dopamine-containing neurons in the ventral tegmental area is necessary for the reinforcing effects of opioids and other abused drugs. Intracellular recordings from these cells in slices of rat brain in vitro showed that opioids do not affect the principal (dopamine-containing) neurons but hyperpolarize secondary (GABA-containing) interneurons. Experiments with agonists and antagonists selective for opioid receptor subtypes indicated that the hyperpolarization of secondary cells involved the mu-receptor. Most principal cells showed spontaneous bicuculline-sensitive synaptic potentials when the extracellular potassium concentration was increased from 2.5 to 6.5 or 10.5 mM; these were prevented by TTX and assumed to result from action potentials arising in slightly depolarized local interneurons. The frequency of these synaptic potentials, but not their amplitudes, was reduced by opioids selective for mu-receptors. It is concluded that hyperpolarization of the interneurons by opioids reduces the spontaneous GABA-mediated synaptic input to the dopamine cells. In vivo, this would lead to excitation of the dopamine cells by disinhibition, which would be expected to contribute to the positive reinforcement seen with mu-receptor agonists such as morphine and heroin.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗