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Results for “Synaptic Potentials”

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At least 181 records · Page 10Linked to original sources

PubMed1995

Synaptic potentiation of dual-component excitatory postsynaptic currents in the rat hippocampus.

1. Whole-cell patch-clamp recording has been used to study tetanus-induced synaptic potentiation of dual-component excitatory postsynaptic currents (EPSCs) in the CA1 region of rat hippocampal slices, following blockade of GABAA and GABAB receptor-mediated synaptic inhibition. 2. At a holding potential of -60 mV, the initial slope of the EPSC (between 10 and 60% of maximum amplitude) provided an accurate measurement of the AMPA receptor-mediated component, and the amplitude of the EPSC at a latency of 100 ms provided the best estimate of the size of the NMDA receptor-mediated component. 3. Neurons were voltage clamped for at least 45 min prior to delivery of a tetanus (test intensity, 100 Hz, 1 s). Measurements at 10 and 30 min following the tetanus were used as indications of short-term potentiation (STP) and long-term potentiation (LTP), respectively. One set of neurons were voltage clamped at -60 mV throughout. These neurons could be subdivided into two populations on the basis of whether or not there was LTP (n = 9), or only STP (n = 6), of the AMPA receptor-mediated component. A second set of neurons were voltage clamped at -60 mV for 30 min and then at -50 mV for 15 min before, during and for 30 min following tetanization. In these experiments there was STP but not LTP (n = 8). 4. In all neurons (n = 23), the time course of the potentiation of the NMDA receptor-mediated component paralleled that of the AMPA receptor-mediated component. In addition, potentiation of the NMDA and AMPA receptor-mediated components were of a similar magnitude. 5. These data demonstrate that it is possible to induce LTP by high frequency stimulation after 45 min of whole-cell recording. Under these conditions, there is a parallel potentiation of the AMPA and NMDA receptor-mediated components of dual-component EPSCs. This constitutes the first evidence, from studies of dual-component synaptic responses, which is consistent with a presynaptic locus of expression of tetanus-induced STP and LTP in the hippocampus.

Animals↗

PubMed2000

Influence of the size of syncytial units on synaptic potentials in smooth muscle.

The effect of the size of syncytial bundles of cells on the passive synaptic potentials generated within them has been explored. Computer simulations have been performed of neuronally produced spontaneous excitatory junction potentials (SEJPs) generated in cubical 'bidomain' model of syncytial tissue. It is found that indical properties of SEJPs vary conspicuously in syncytium sizes smaller than about 15-17-cube, but change very little in syncytium sizes greater than this. At the centroid of the cube, the peak amplitude Vp of the SEJP declines from 14.32 mV to 11.70 mV as syncytium size increases from 7-cube to 15-cube, i.e. a decrease of approximately 18%, while between system sizes 15-cube (Vp = 11.70 mV) and 29-cube (Vp = 11.67 mV), the reduction is only approximately 0.3%. Similar trends are observed for the time to peak of SEJPs. These observations indicate a minimum bundle size in smooth muscle below which syncytial function is modified; the implications of this are discussed.

Computer Simulation↗

PubMed1990

A 1-heteroaryl-4-piperidinyl-methyl pyrrolidinone, BMY 21502, delays the decay of hippocampal synaptic potentiation in vitro.

The effects of the substituted pyrrolidinone, BMY 21502, on the properties of cell membranes, synaptic transmission and synaptic plasticity, were assessed in area CA1 of hippocampal slices from the rat. Application of the compound to the bath had no consistent direct effects on parameters of the cell membrane or evoked synaptic potentials, at concentrations of less than 30 microM. In a blind experimental design, BMY 21502 at 1.0 and 10 microM, but not 25 microM, significantly delayed the decay of long-term potentiation in slices obtained from young animals; in slices obtained from very old rats (2.5-3.2 yr), 10 microM BMY 21502 significantly delayed decay of long-term potentiation. Therefore BMY 21502 was active in a physiological model that may predict of cognitive enhancement.

Aging↗

PubMed1994

Effect of mannose, fructose and lactate on the preservation of synaptic potentials in hippocampal slices.

We investigated the effect of fructose, mannose and lactate on the preservation of synaptic transmission in the granule cell layer of guinea pig hippocampal slices during deprivation of glucose. After replacement of glucose with lactate (5 mM) or fructose (10 mM), population spikes (PS) extinguished transiently and thereafter recovered to 60-70% of the original amplitude. Replacement of glucose with mannose (10 mM) decreased the PS amplitude by 50-60% within 20 min. and was followed by recovery to 80% of the original amplitude. The levels of ATP and CrP (creatine phosphate) in fructose, mannose and lactate containing medium were maintained at 80-90% of the original levels. PS of the slices exposed to both glucose and lactate showed a similar pattern to that observed in lactate medium with deprivation of glucose. These results suggest that lactate, mannose and fructose could be metabolic substrates for energy production and are able to preserve the synaptic potentials, however, it takes 20-30 min for the functional replacement of glucose with these sugars or metabolites to occur.

Adenosine Triphosphate↗

PubMed1999

Presynaptic mechanism for phorbol ester-induced synaptic potentiation.

Phorbol ester facilitates transmitter release at a variety of synapses, and the phorbol ester-induced synaptic potentiation (PESP) is a model for presynaptic facilitation. To address the mechanism underlying PESP, we have made paired whole-cell recordings from the giant presynaptic terminal, the calyx of Held, and its postsynaptic target in the medial nucleus of the trapezoid body in rat brainstem slices. Phorbol ester potentiated EPSCs without affecting either presynaptic calcium currents or potassium currents. Protein kinase C inhibitors applied from outside or injected directly into the presynaptic terminal attenuated the PESP. Furthermore, presynaptic loading of a synthetic peptide with the sequence of the N-terminal domain of Doc2alpha interacting with Munc13-1 (Mid peptide) significantly attenuated PESP, whereas mutated Mid peptide had no effect. We conclude that the target of the presynaptic facilitatory effect of phorbol ester resides downstream of calcium influx and may involve both protein kinase C and Doc2alpha - Munc13-1 interaction.

Amino Acid Sequence↗

PubMed1988

Enkephalin analogues depress synaptic potentials in rat dentate granule cells recorded intracellularly in vitro.

Enkephalin analogues were superfused onto hippocampal slices during intracellular recording of dentate granule cells. The enkephalins elicited either weak depolarizations, weak hyperpolarizations, or no effect on membrane potential, in about equal numbers of cells tested. Similarly, input resistance either decreased, increased or did not change, and was not well correlated with the potential changes. However, at all concentrations tested (2-10 microM) the enkephalins reduced evoked depolarizing synaptic potentials by up to 70%. We speculate that a major function of endogenous enkephalin-containing fibers projecting to the dentate is to dampen afferent synaptic transmission.

Action Potentials↗

PubMed1998

PGE2 hyperpolarizes gallbladder neurons and inhibits synaptic potentials in gallbladder ganglia.

Gallbladder prostaglandin E2 (PGE2) levels are significantly elevated in pathophysiological conditions, resulting in changes in gallbladder motility or secretion that may involve actions of the prostanoid in intramural ganglia. This study was undertaken to examine the effects of PGE2 on neurons of the intramural ganglia of the guinea pig gallbladder. Application of PGE2 by microejection or superfusion elicited a complex triphasic change in the resting membrane potential (RMP). For example, application of PGE2 by microejection (100 microM) resulted in a brief hyperpolarization (mean duration 11.1 +/- 1.3 s), followed by a mid-phase repolarization toward or above RMP (mean duration 50.7 +/- 8.1 s), and finally a long-lasting hyperpolarization (mean duration 157.3 +/- 36.7 s). Associated with these PGE2-evoked alterations in RMP were changes in input resistance measured via injection of hyperpolarizing current pulses. An examination of the action potential afterhyperpolarization (AHP) during the PGE2-evoked response revealed an attenuation of both the amplitude and duration of the AHP. However, only a slight increase in excitability of gallbladder neurons in the presence of PGE2 was evident in response to depolarizing current pulses, and PGE2 did not cause the cells to fire spontaneous action potentials. Application of PGE2 reduced the amplitudes of both fast and slow excitatory synaptic potentials. These results suggest that increased prostaglandin production may decrease ganglionic output and therefore contribute to gallbladder stasis.

Animals↗

PubMed1985

Quantal mechanism of long-term synaptic potentiation.

Intracellular recordings were used to demonstrate the occurrence and to analyze the microphysiology of long-term synaptic potentiation (LTP) in the crayfish opener neuromuscular synapse. Brief stimulation of the single excitor motor axon enhanced the amplitudes of subsequent postsynaptic potentials for several hours. Three methods of quantal analysis were used to evaluate the mechanism responsible for LTP. The results of all three methods supported predictions of the hypothesis that LTP results from a presynaptic mechanism that increases the average of neurotransmitter quanta evoked by nerve impulses in the excitor axon.

Animals↗

PubMed1978

Adaptive rundown of excitatory post-synaptic potentials at synapses between hair cells and eight nerve fibres in the goldfish.

1. The excitatory post-synaptic potentials (e.p.s.p.s.) evoked by sound stimuli were recorded intracellularly from large afferent eight nerve fibres in the sacculus of the goldfish (S1 fibres). The fish were anaesthetized with MS-222 and spike potentials were suppressed with locally applied tetrodotoxin. 2. The e.p.s.p.s. successively evoked in response to each wound wave showed a marked rundown in size, while no reduction was observed in the microphonic potentials. The amplitude of successive e.p.s.p.s was reduced keeping approximately a fixed ratio to the preceding ones, suggesting that the rundown is attributable to a depletion of transmitter quanta from the release sites. 3. The rate of rundown of successive e.p.s.p.s, however, remained almost unchanged when the intensity of the stimulus sound was changed. It was also observed that, even after the e.p.s.p.s had been completely adapted to a continuous sound, a vigorous discharge of new e.p.s.p.s was observed when the intensity of the sound was increased. 4. These findings seem to indicate that it is the size of the readily available store and not the release fraction that is changed by a change in the sound intensity. 5. The saccular macula was superfused with solutions different in Ca and Mg ion concentrations. High Ca ion concentration brought about an increase in the size of the readily available store as well as the release fraction. 6. Mechanisms underlying these observations were discussed in terms of the quantal release mechanism as well as the morphology of the release sites.

Acoustic Stimulation↗

PubMed1987

Presynaptic inhibition of synaptic potentials evoked in cat spinal motoneurones by impulses in single group Ia axons.

1. Single-fibre group Ia excitatory post-synaptic potentials (e.p.s.p.s) were evoked in triceps surae motoneurones. These e.p.s.p.s were reduced by conditioning stimulation of group I axons in posterior biceps-semitendinosus nerves. 2. The investigation concentrated on e.p.s.p.s of somatic origin, because the amplitude of these e.p.s.p.s is not reduced by post-synaptic conductance increases. Any reduction in these e.p.s.p.s could therefore be attributed to presynaptic inhibition. 3. The reduction in somatic e.p.s.p. amplitude was greatest when the conditioning stimulus preceded the e.p.s.p. by 30 ms, and was negligible when the conditioning interval was extended to 200-300 ms. 4. The percentage reduction of somatic e.p.s.p.s was independent of their unconditioned peak amplitude. 5. E.p.s.p.s of somatic origin were reduced by the same amount, on average, as e.p.s.p.s of dendritic origin. 6. E.p.s.p.s evoked in the same motoneurone by impulses in different Ia axons were reduced by different amounts and e.p.s.p.s evoked in different motoneurones by impulses in the same Ia axon were also reduced by different amounts. 7. Analysis of fluctuations in e.p.s.p.s before and after conditioning indicated that after conditioning, larger discrete amplitudes became less probable, while smaller discrete amplitudes became more probable. The average increment between discrete amplitudes did not alter; nor were the discrete amplitudes reduced. 8. The probabilities of transmitter release at synaptic boutons were calculated before and during presynaptic inhibition. The maximum decrease in release probability was 0.64, suggesting a reduction in calcium influx of 10-15%.

Animals↗

PubMed1981

Analysis of synaptic potentials in mitral cells in the isolated turtle olfactory bulb.

1. The synaptic responses of mitral cells have been analysed in intracellular recordings from the isolated olfactory bulb of the turtle. 2. The response of a mitral cell to a single volley in the lateral olfactory tract consisted of and antidromic impulse and a complex hyperpolarizing potential that had the properties of an inhibitory post-synaptic potential. The inhibitory response consisted of two successive components I1 and I2, followed by a prolonged hyperpolarization. 3. High-gain recordings revealed miniature hyperpolarizing potentials during the I1 and I2 responses. Both the miniature potentials and the I1 and I2 responses were increased in amplitude by depolarizing injected currents, and decreased and reversed in polarity by hyperpolarizing currents. The input conductance was increased during the I2 component. In some cells the I1 and I2 components, recorded with micropipettes filled with potassium acetate or potassium citrate, were depolarizing. 4 A single orthodromic volley in the olfactory nerves elicited a complex depolarizing-hyperpolarizing potential in mitral cells. The depolarization consisted of two successive components, E1 and E2. The hyperpolarization consisted of two successive components, I1 and I2, followed by a prolonged hyperpolarization. 5. The depolarizing components had the properties of excitatory post-synaptic potentials. They decreased in amplitude with depolarizing current injection and increased with hyperpolarizing injection. The hyperpolarizing components resembled the I1 and I2 components of the tract-evoked responses in their timing and properties. 6. It is postulated that the E1 component reflects the initial excitation by olfactory nerve terminals of the mitral cell dendritic tufts in the olfactory glomeruli. The I1 component is postulated to arise from dendrodendritic synaptic input mediated by interneurones, mainly granule cells. The E2 and I2 components are likely to arise mainly from intrinsic synaptic circuits within the olfactory bulb.

Animals↗

PubMed1991

Ethanol and magnesium ions inhibit N-methyl-D-aspartate-mediated synaptic potentials in an interactive manner.

The role of magnesium ions in the inhibitory effect of ethanol on NMDA receptor-mediated population synaptic potentials (pEPSPs) in area CA1 of the hippocampus of the adult rat, was studied. The excitatory amino acid (non-NMDA) receptor antagonist, DNQX and the GABAA channel antagonist, picrotoxin, were used to pharmacologically isolate NMDA-mediated pEPSPs. In the presence of a physiological concentration of magnesium (1.0 mM), ethanol (25-100 mM) inhibited NMDA-mediated pEPSPs, with an apparent EC50 of approximately 50 mM. The ability of ethanol to inhibit NMDA-mediated pEPSPs was reduced when the slices were incubated in the absence of magnesium. Concentrations of ethanol, in the range of 50-200 mM (apparent EC50 100 mM), were required to inhibit NMDA-mediated pEPSPs, in the absence of added magnesium. Combination studies of these two antagonists indicated that the sensitivity of NMDA-mediated pEPSPs to one antagonist was not altered by the presence of the other. This finding suggests that the affinity of each antagonist binding site is not affected by the presence of the other antagonist. In the case of ethanol, its low maximum antagonist efficacy may require larger concentrations of ethanol to inhibit NMDA-mediated pEPSPs, in the absence of other non-competitive antagonists such as magnesium.

Animals↗

PubMed1992

Neuropeptide Y selectively inhibits slow synaptic potentials in rat dorsal raphe nucleus in vitro by a presynaptic action.

Neuropeptide Y (NPY) has been shown to modulate synaptic transmission in both peripheral and central tissues via both pre- and postsynaptic mechanisms. In this study, we examined the effect of NPY and its analog, peptide YY (PYY), on slow synaptic potentials in the dorsal raphe nucleus in vitro using intracellular recording and single-microelectrode voltage-clamp techniques. NPY and PYY inhibited both the slow 5-HT1A receptor-mediated IPSP and the alpha 1-adrenoceptor-mediated slow EPSP while not affecting the fast, amino acid-mediated synaptic responses. PYY also inhibited pharmacologically isolated slow synaptic responses. NPY/PYY appear to mediate the observed inhibitions via a presynaptic mechanism, as the postsynaptic conductances mediated by activation of 5-HT1A receptors or alpha 1-adrenoceptors were unaffected by the peptides. NPY/PYY act via a different mechanism than presynaptic 5-HT1B receptors. NPY/PYY probably act via presynaptic Y2 receptors, as the C-terminal fragment NPY 13-36 and the Y2-selective agonist C2-NPY are effective. Since NPY and its receptors are present in the dorsal raphe nucleus, this peptide may act as an endogenous modulator of the state of activity of neurons in this region and may thus have a role in the modulation of neuronal output from this nucleus.

Animals↗

PubMed1999

Evidence that inhibitory motor neurons of the guinea-pig small intestine exhibit fast excitatory synaptic potentials mediated via P2X receptors.

Intracellular recordings were used to study the contribution of nicotinic and P2X receptors to synaptic transmission to morphologically identified myenteric neurons of guinea-pig ileum. Hexamethonium (100 microM) abolished fast excitatory synaptic potentials (EPSPs) in all orally projecting neurons, but fast EPSPs in anally projecting neurons were resistant to this antagonist. The non-cholinergic fast EPSPs were virtually abolished by suramin (100 microM). This suggests that P2X receptors are important in descending motility reflexes. However, suramin and hexamethonium together did not affect descending inhibitory reflexes when applied to the site of transmission between interneurons in this pathway. These data suggest that P2X receptors are not involved in transmission between descending interneurons, but may be important for transmission to inhibitory motor neurons.

Animals↗

PubMed2002

Slow excitatory synaptic potentials evoked by distension in myenteric descending interneurones of guinea-pig ileum.

The functional significance of the slow excitatory synaptic potentials (EPSPs) in myenteric neurones is unknown. We investigated this using intracellular recording from myenteric neurones in guinea-pig ileum, in vitro. In all, 121 neurones responded with fast EPSPs to distension of the intestine oral to the recording site. In 28 of these neurones, distension also evoked depolarizations similar to the slow EPSPs evoked by electrical stimulation in the same neurones. Intracellular injection of biocytin and immunohistochemistry revealed that neurones responding to distension with slow EPSPs were descending interneurones, which were immunoreactive for nitric oxide synthase (NOS). Other neurones, including inhibitory motor neurones and interneurones lacking NOS, did not respond to distension with slow EPSPs, but many had slow EPSPs evoked electrically. Slow EPSPs evoked electrically or by distension in NOS-immunoreactive descending interneurones were resistant to blockade of NK(1) or NK(3) tachykinin receptors (SR 140333, 100 nM; SR 142801, 100 nM, respectively) and group I metabotropic glutamate receptors (PHCCC, 10-30 microM), when the antagonists were applied in the recording chamber of a two-chambered organ bath. However, slow EPSPs evoked electrically in inhibitory motor neurones were substantially depressed by SR 140333 (100 nM). Blockade of synaptic transmission in the stimulation chamber of the organ bath abolished slow EPSPs evoked by distension, indicating that they arose from activity in interneurones, and not from anally directed, intrinsic sensory neurones. Thus, distension evokes slow EPSPs in a subset of myenteric neurones, which may be important for intestinal motility.

Animals↗

PubMed2000

Time-sharing contributions of A- and D-type K+ channels to the integration of high-frequency sequential excitatory post synaptic potentials at a model dendrite in rats.

A- and D-type K+ channels (KA and KD channels) have unique physiological properties that play important roles in the integration of excitatory post synaptic potentials (EPSPs) in neuronal dendrites. These functions were analyzed using a computer program, NEURON, to simulate high-frequency sequential synaptic inputs, that can induce long-term potentiation (LTP). We paid close attention to the stability of the reduction of sequential EPSPs. When either KA or KD channels were included in models, the EPSP reduction ratios were less stable than containing both KA and KD channels. When both KA and KD channels were present in the model, the variance of EPSP reduction ratios was significantly smaller in comparison with that in the presence of either KA or KD channels alone. We thus concluded that the co-existence of KA and KD channels is necessary to produce stable EPSPs during the high-frequency synaptic stimulation necessary for induction of LTP.

Animals↗

PubMed1998

Temporal correlation between adenosine outflow and synaptic potential inhibition in rat hippocampal slices during ischemia-like conditions.

The temporal correlation between adenosine outflow and changes in field excitatory post synaptic potentials (fEPSP) occurring during ischemia-like conditions was investigated in rat hippocampal slices. Five-minute long ischemia-like conditions resulted in a 100% depression of fEPSP amplitude, followed by a complete recovery after 6-7 min of reperfusion. By reducing the duration of the ischemic insult to 2 min, fEPSP was depressed by 50%. During both 5 and 2 min of ischemia-like conditions, a significant increase in adenosine outflow was detected. During reperfusion, when fEPSP amplitude recovered completely, the adenosine level in the extracellular fluid returned to basal values. The strict relationship between the increase in adenosine outflow and fEPSP inhibition supports the hypothesis that adenosine is largely responsible for the synaptic transmission depression during cerebral ischemia.

Adenosine↗

PubMed1994

Inhibitory synaptic potentials in guinea-pig substantia nigra dopamine neurones in vitro.

1. The properties of stimulus-evoked and spontaneous inhibitory synaptic potentials were examined in guinea-pig substantia nigra dopamine neurones in sagittal and coronal midbrain slices in the presence of glutamate receptor antagonists. 2. Focal electrical stimulation within the substantia nigra, cerebral peduncle, internal capsule or the striatum evoked a biphasic IPSP consisting of a fast and a slow component, with peak latencies of about 30 and 250 ms, respectively. The fast component was sensitive to chloride injection, reversed polarity at -79.4 +/- 1.1 mV and was blocked by the GABAA receptor antagonists picrotoxin and bicuculline. The slow IPSP reversed at -99.3 +/- 5.4 mV and was blocked by the GABAB receptor antagonists 2-hydroxysaclofen and CGP 35348. 3. Spontaneous IPSPs were observed in many neurones. These events reversed polarity at -77.5 +/- 2.6 mV and were completely blocked by bicuculline and/or picrotoxin. In the presence of TTX, small spontaneous events remained which probably represent miniature IPSPs. In coronal slices, application of 4-aminopyridine raised the frequency of spontaneous IPSPs, presumably by activating nigral interneurones, but failed to reveal spontaneous biphasic IPSPs or spontaneous pure slow IPSPs. 4. The amplitude of the fast IPSPs fluctuated from trial to trial. Amplitude histograms of minimal fast IPSPs displayed evenly spaced peaks, suggesting that synaptic transmission is quantal at these synapses. The measured peak spacing depended on the driving force for Cl-. 5. The fast IPSP showed little or no paired-pulse depression, and in the presence of 2-hydroxysaclofen (400-600 microM) showed paired-pulse facilitation. The GABAB agonist baclofen inhibited the fast IPSP via a presynaptic mechanism. The pharmacologically isolated slow IPSP showed marked paired-pulse facilitation. 6. It is concluded that synaptic inhibition in the substantia nigra is mediated by GABA, is relatively resistant to frequency-dependent depression and is regulated by presynaptic GABAB autoreceptors. Striatonigral and pallidonigral fibres activate both GABAA and GABAB receptors, while intranigral pathways appear to activate predominantly GABAA receptors.

Animals↗