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 487 records · Page 27Linked to original sources
PubMed1992

Antagonism of synaptic potentials in ventral horn neurones by 6-cyano-7-nitroquinoxaline-2,3-dione: a study in the rat spinal cord in vitro.

1. The rat spinal cord in vitro has been used to assess the effect of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) on the dorsal root evoked extracellular ventral root reflex (DR-VRR) and the intracellular excitatory postsynaptic potential (e.p.s.p.) in ventral horn neurones and motoneurones. 2. CNQX (1-5 microM) produces a selective and dose-dependent reduction in the amplitude of the monosynaptic component of the DR-VRR recorded from lumbar spinal segments. 3. With low intensity dorsal root stimulation CNQX selectively attenuates the amplitude of the short latency intracellular e.p.s.p. (70% reduction, P < 0.005) and its rise-time (75%, P < 0.01) without affecting the half-time to decay. 4. When high intensity stimulation is used CNQX significantly attenuates the amplitude of the e.p.s.p. (56%, P < 0.005), rise-time (76%, P < 0.01) and abolishes the short latency spike. In addition longer latency synaptic components are attenuated and the half-time to decay significantly reduced (47%, P < 0.005). 5. The results with CNQX are compared to D-aminophosphonovalerate and discussed in relation to the recruitment of low versus high threshold afferents. The data supports an involvement of non-NMDA receptors in transmission through both mono- and polysynaptic pathways in the ventral horn.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Quantal behaviour of synaptic transmission can be statistically examined using the Fourier line spectrum of the histogram of synaptic potentials.

A statistical approach to reveal the quantal behaviour of postsynaptic potentials (PSPs) is described. This includes: (1) obtaining the Fourier line spectrum (decomposition into harmonics) of the PSP histogram; and (2) testing the null hypothesis, 'the spectrum is that of white noise', using an ANOVA. The harmonic that rejects the hypothesis will indicate the regular peaks in the histogram, i.e., the quantal size of PSPs. The method was tested using published results of three experimental studies in central synapses and yielded the quantal sizes close to those derived from other methods. However, using three examples of published simulation studies (where the quantal model of synaptic transmission was known a priori), it was shown that the approach can estimate quantal sizes of PSPs more reliably than other methods.

Analysis of Variance↗
PubMed1996

The synaptic potential mediated by metabotropic glutamate receptors is not associated with a substantial elevation of cytosolic free calcium concentration in Purkinje cells.

Brief tetanic stimulation of parallel fibres can evoke a slow excitatory postsynaptic potential (EPSP) in cerebellar Purkinje cells that is mediated by metabotropic glutamate receptors (mGluRs). It is likely that the receptor subtype involved is mGluR1, which couples to the production of diacylglycerol and inositol-1,4,5-trisphosphate (IP3). We therefore examined whether the mGluR-EPSP is associated with an increase in cytosolic free calcium [Ca2+]i using simultaneous Ca2+ imaging and electrophysiological recordings. An mGluR-EPSP could be evoked in all nine Purkinje cells tested. In all but one this potential was not associated with measurable changes in [Ca2+]i whereas single calcium spikes produced large Ca2+ transients. In the one Purkinje cell where [Ca2+]i was elevated, the rise was estimated to be roughly 20-fold smaller than that produced by a single Ca2+ spike.

Animals↗
PubMed1996

Properties of convergent thalamocortical and intracortical synaptic potentials in single neurons of neocortex.

We explored differences in the properties of convergent afferent inputs to single neurons in the barrel area of the neocortex. Thalamocortical slices were prepared from mature mice. Recordings were made from neurons in layer V, and either thalamocortical afferents or horizontal intracortical axons were stimulated. Monosynaptic EPSPs from both sources had latencies shorter than 1.8 msec and low shape variance. Disynaptic thalamocortical IPSPs had latencies longer than 1.8 msec. All neuronal types, as defined by intrinsic firing patterns, received both thalamocortical and intracortical monosynaptic input. The shape parameters (rate of rise and half-width) of monosynaptic EPSPs from the two inputs did not differ significantly. The rate of rise of EPSPs varied considerably across cells, but the rates of rise of thalamocortical and intracortical EPSPs onto single cells were strongly correlated. The relative thresholds for activation of synaptic excitation and inhibition were strikingly different between the two tracts: thalamocortical stimulation induced GABAA-dependent IPSPs at stimulus intensities equal to or less than those required for evoking EPSPs in 35% (24 of 68) of the cells. In contrast, the threshold response to intracortical stimulation was always an EPSP, and only stronger stimuli could generate di- or polysynaptic IPSPs. We suggest that postsynaptic factors may tend to equalize the waveforms of EPSPs from thalamocortical and intracortical synapses onto single neurons. A major difference between the two convergent tracts is that the thalamocortical pathway much more effectively activates feedforward inhibitory circuits than does the horizontal intracortical pathway.

Animals↗
PubMed1992

Quinoxaline derivatives: structure-activity relationships and physiological implications of inhibition of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated currents and synaptic potentials.

The inhibitory potencies at excitatory amino acid (EAA) receptors of 11 quinoxaline derivatives were evaluated in two-electrode voltage-clamp recordings of Xenopus oocytes injected with rat cortex mRNA. Currents activated by kainate or (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) in Xenopus oocytes were inhibited competitively by all the quinoxaline derivatives, with apparent Ki values ranging from 0.27 to 300 microM against kainate and from 0.25 to 137 microM against AMPA. An excellent correlation was observed between inhibitory potencies of the quinoxaline derivatives against kainate and AMPA currents, in support of the contention that in this preparation these two agonists act at a single site. All 11 quinoxaline derivatives also inhibited current activated by the combination of glycine and N-methyl-D-aspartate (NMDA), apparently acting at the glycine site, and did so over a narrower range of apparent Ki values (0.37-8.1 microM). The correlation between the quinoxalines' kainate/AMPA potencies and their glycine/NMDA potencies was relatively weak. Thus, the quinoxaline derivatives were all good antagonists of glycine/NMDA currents and displayed a greater range of potencies against kainate and AMPA. The inhibitory effects of the six quinoxaline derivatives most potent in the Xenopus oocyte experiments were also tested against the excitatory postsynaptic field potential (EPSFP) recorded in the pyramidal cell dendritic field of the CA1 region of hippocampal slices after stimulation of the Schaffer collateral-commissural pathways. In slices superfused with "normal" medium (containing 1 mM Mg2+), in which the EPSFP is mediated primarily by non-NMDA receptors, IC50 values correlated closely with the Ki values against kainate/AMPA obtained in oocyte experiments but were approximately 8-fold higher. Similarly, in slices superfused with nominally Mg(2+)-free medium, in which the EPSFP is amplified due to a relief of the Mg2+ block of NMDA receptors, IC50 values correlated closely with the Ki values against glycine/NMDA obtained in oocyte experiments but were 60-fold higher. This comparison of results from the two experimental systems lends further support to the argument that hippocampal synaptic transmission is mediated postsynaptically by kainate/AMPA-type and NMDA/glycine-type EAA receptors that are pharmacologically indistinguishable from those expressed in mRNA-injected Xenopus oocytes. Furthermore, it suggests that EAA receptors in situ may be nearly saturated by high local concentrations of the endogenous ligands, a condition that would contribute substantially to the apparent non-NMDA receptor selectivity of certain quinoxaline derivatives.

Animals↗
PubMed1995

Preparation of carbon-fibre microelectrode for extracellular recording of synaptic potentials.

A method is proposed for rapid and effective forming of the recording tips of carbon-fibre microelectrodes by trimming and treating the tip with electric current pulses. The tip is trimmed to the required length. The signal-to-noise ratio of carbon-fibre microelectrodes is improved at low-frequency range (less than 100 Hz) after the treatment. The same microelectrode may be used for several experiments because of the possibility to trim and treat the tips repeatedly. This method also allows one to readily fabricate 2- or multi-channel carbon-fibre microelectrodes with the vertical distance between recording tips from few tens to hundreds of micrometres. As an example, the process of fabrication of a 2-channel microelectrode is described.

Carbon↗
PubMed1999

Presynaptic inhibition of GABA(B)-mediated synaptic potentials in the ventral tegmental area during morphine withdrawal.

Opioids increase the firing of dopamine cells in the ventral tegmental area by presynaptic inhibition of GABA release. This report describes an acute presynaptic inhibition of GABAB-mediated IPSPs by mu- and kappa-opioid receptors and the effects of withdrawal from chronic morphine treatment on the release of GABA at this synapse. In slices taken from morphine-treated guinea pigs after washing out the morphine (withdrawn slices), a low concentration of a mu receptor agonist increased, rather than decreased, the amplitude of the GABAB IPSP. In withdrawn slices, after blocking A1-adenosine receptors with 8-cyclopentyl-1, 3-dipropylxantine, mu-opioid receptor activation inhibited the IPSP at all concentrations and increased the maximal inhibition. In addition, during withdrawal, there was a tonic increase in adenosine tone that was further increased by forskolin or D1-dopamine receptor activation, suggesting that metabolism of cAMP was the source of adenosine. The results indicate that during acute morphine withdrawal, there was an upregulation of the basal level of an opioid-sensitive adenylyl cyclase. Inhibition of this basal activity by opioids had two effects. First, a decrease in the formation of cAMP that decreased adenosine tone. This effect predominated at low mu receptor occupancy and increased the amplitude of the IPSP. Higher agonist concentrations inhibited transmitter release by both kinase-dependent and -independent pathways. This study indicates that the consequences of the morphine-induced upregulation of the cAMP cascade on synaptic transmission are dependent on the makeup of receptors and second messenger pathways present on any given terminal.

Adenosine↗
PubMed1995

Cocaine prolongs norepinephrine synaptic potentials in rat dorsal raphe.

1. The effect of cocaine on the excitatory response to norepinephrine (NE) was investigated with the use of intracellular recording from rat dorsal raphe (DR) neurons in the slice preparation. 2. Focal stimulation evoked a slow excitatory postsynaptic potential (sEPSP) that was mediated by alpha 1-adrenoceptor activation. The sEPSP was studied in isolation with the use of a selective 5-HT1A receptor antagonist, pindobind 5HT1A, which eliminated the inhibitory postsynaptic potential (IPSP) that preceded the sEPSP. The sEPSP had a latency to peak of 6 s, a peak amplitude of 6 mV, and a time constant of decay (t) of 14 s. 3. Bath application of cocaine more than doubled the latency-to-peak (13 s) and the time constant of decay (29 s) and had no effect on the amplitude. 4. Iontophoretically applied NE produced a membrane potential depolarization with an amplitude and time course similar to the sEPSP (latency-to-peak = 10 s; peak amplitude = 5 mV; t = 20 s). Cocaine significantly increased the latency-to-peak and the time constant of decay of the depolarization induced by iontophoretically applied NE. 5. Superfusion with NE caused a concentration-dependent depolarization. Cocaine (1 microM) did not change the concentration response to NE. 6. These results suggest that cocaine enhances the excitatory action of NE in the dorsal raphe by a prolongation of the alpha 1-adrenoceptor-mediated sEPSP.

Animals↗
PubMed1996

Reverberation of chloride-dependent synaptic potentials in the rat entorhinal cortex in vitro.

The spontaneous activity generated by rat entorhinal neurons during application of 4-aminopyridine (4AP; 50 microM) was studied with intracellular and extracellular field-potential recordings in an vitro slice preparation. Long-lasting depolarizations (LLDs) with amplitudes of 15 +/- 7.6 mV (mean +/- SD; n = 14) and durations of 1.65 +/- 0.77 s (n = 14) occurred at 0.036 +/- 0.01/s (n = 14). Each LLD was followed by a rhythmic sequence of depolarizing potentials (up to 22 events) with amplitudes of 4-30 mV, durations of 40-500 ms and frequency of 0.9 +/- 0.2/s (n = 14). These intracellular potentials were mirrored by negative-going field potentials, suggesting that they represented synchronous events. Membrane input resistance decreased by 79-86% during both LLDs and subsequent rhythmic depolarizations. Intracellular injection of steady depolarizing or hyperpolarizing current modified the amplitude of these potentials in a similar manner: the reversal potential of the LLDs and of the rhythmic depolarizations was -66.4 +/- 4 mV and -67.9 +/- 3.2 mV, respectively (n = 7). Intracellular injection of Cl- increased the amplitude of both types of potentials. Spontaneous LLDs continued to occur during application of the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione (10 microM), a procedure that abolished the subsequent rhythmic depolarizations (n = 3). LLDs were blocked by further addition of the gamma-aminobutyric acid (GABA)A receptor antagonist bicuculline methiodide (10 microM, n = 3). Our findings demonstrate that during 4AP application entorhinal neurons generate glutamatergic-independent LLDs as well as synchronous, Cl(-)-dependent depolarizations that reverberate through non-NMDA-mediated excitatory circuits.

4-Aminopyridine↗
PubMed1995

On the contribution of quantal secretion from close-contact and loose-contact varicosities to the synaptic potentials in the vas deferens.

A bidomain model of the smooth muscle syncytium has been used to analyse the sources of transmitter secretion that give rise to the excitatory junction potential (EJP) in the guinea-pig vas deferens. The timecourse of the spontaneous excitatory junction potential (SEJP) has been taken to be the same as the time course of action of a quantum of transmitter. The amplitude of the SEJP is dependent on both the size of the quantum secreted and the distance away of the source of the quantum from the muscle cells. Two such sources are considered, one identified as the close-contact varicosities (CCVS) about 50 nm from the muscle and the other as loose-contact varicosities (LCVS) at greater distances. It is shown that in order for the syncytium to reach equipotential by the time the EJP has declined to about 80% of its peak, each muscle cell must receive a quantum of transmitter. The relatively low density of innervation of muscle cells by CCVS so far reported, together with the extremely low probability for secretion from these, indicates that many LCVS surrounding each muscle cell contribute to the EJP. The rising phase of the EJP contains components that indicate the sources of the transmitter responsible for its generation, and these components have been made explicit by differentiating the EJP to give the DEJP. This always has a smooth and relatively slow component that lasts for about 80 to 100 ms and occasionally has fast components superimposed on it. These latter are shown to be almost certainly due to secretion of quanta from the CCVS. It is known that there is a distribution of action potential velocities in the sympathetic nerves to the vas deferens. To account for this, the secretion of quanta from different CCVS on a set of muscle cells in the syncytium were given different delays so that the DEJP consisted of a slow wave form that extended over 80 ms, composed of clearly discernible components arising from the CCVS. This wave form could be smoothed by allowing each cell in the syncytium to receive a quantum of transmitter from a CCV, a condition that did not then allow for the appearance of fast components in the DEJP. A model that generated both the non-intermittent slow component of the DEJP and the intermittent fast component consisted of each cell in the syncytium receiving an innervation from a single CCV as well as from a large number of LCVS. In this case, all the varicosities could secrete a quantum of transmitter with a particular probability after a delay characteristic for that varicosity.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗
PubMed1986

[Paired facilitation of the summated extracellular synaptic potentials of individual retino-tectal fibers in the frog].

The paired-pulse facilitation of the EEG quanta (the extracellular monosynaptic PSPS of all synapses of one axon) was examined in layer F of the frog tectum at normal and at increased concentrations of external Ca or Mg ions. The maximum values of facilitation were observed with intervals between stimuli of about 5 ms. Under normal conditions the amount of maximal facilitation was different for separate EEG quanta and varied from 1.4 to 2.4. Distribution of the EEG quanta by the amount of maximal facilitation had two modes at the values fmax = 1.65 and 1.95. The time course of facilitation could be approximated by two exponential components with the time constants of decays tau 1 = 5-6 ms and tau 2 = 140-150 ms for more facilitated EEG quanta, and tau 1 = 6-8 ms and tau 2 = 60-70 ms for the others. Nonequal degree of facilitation of separate EEG quanta and experiments with increased external Ca2+ and Mg2+ concentrations have suggested the dependence of paired-pulse facilitation on the quantum content of the transmitter released in retinotectal synapses. Two types of terminal arbors of axons whose synapses differ in quantum content are supposed to exist in the tectum layer F.

Animals↗
PubMed1993

Hyperpolarizing synaptic potentials evoked in CA1 pyramidal cells by glutamate stimulation of interneurons from the oriens/alveus border of rat hippocampal slices. I. Electrophysiological response properties.

To examine the inhibitory postsynaptic potentials (IPSPs) elicited in pyramidal cells by interneurons situated at the stratum oriens/alveus border (O/A), glutamate was applied by micropressure to this area during intracellular recordings from CA1 pyramidal cells. Glutamate stimulation evoked IPSPs (glut-IPSPs) of small amplitude (4 mV), delayed peak latency (100-110 ms), and long duration (300-400 ms). Recurrent activation of interneurons via glutamate stimulation of pyramidal cells by local application in stratum pyramidale (PYR) evoked recurrent IPSPs (PYR glut-IPSPs) with similar amplitude and time course as O/A glut-IPSPs. The mean equilibrium potential of O/A glut-IPSPs (-77 mV) was significantly different from that of the PYR glut-IPSPs (-71 mV), however, neither equilibrium potential was significantly different from that of the electrically evoked early IPSP in the same cells. Glutamate-evoked IPSPs elicited from O/A displayed some response reversal (27% reversal) like those evoked from PYR (41% reversal). The early IPSP evoked by electrical stimulation displayed significantly more response reversal (67% reversal) than glut-IPSPs. Both types of glut-IPSPs (O/A and PYR) were associated with moderate increases in membrane conductance (5.9 and 6.6 nS, respectively), which were significantly less than the conductance change associated with the early IPSP (45.8 nS). In interneurons within PYR, glutamate stimulation in PYR readily elicited a flurry of excitatory postsynaptic potentials, whereas glutamate stimulation in O/A elicited IPSPs. The electrophysiological properties of IPSPs elicited in pyramidal cells by glutamate stimulation of interneurons in O/A were similar to those of recurrent IPSPs evoked from PYR. Given that both of these types of glutamate-evoked IPSPs were mostly mediated via GABAA receptor channels (Samulack DD, Lacaille J-C, 1993, Hippocampus 3:345-358), the small differences observed between equilibrium potentials, response reversals, and conductance changes could be due to a more electronically distant location from the soma of the synapses involved in O/A glut-IPSPs as compared to those of recurrent IPSPs elicited from PYR.

Animals↗
PubMed1993

Hyperpolarizing synaptic potentials evoked in CA1 pyramidal cells by glutamate stimulation of interneurons from the oriens/alveus border of rat hippocampal slices. II. Sensitivity to GABA antagonists.

The receptor type mediating the inhibitory postsynaptic potentials (glut-IPSPs), recorded in CA1 pyramidal cells, as a result of glutamate stimulation of interneurons in stratum oriens near the alveus (O/A) was assessed and compared to the type mediating recurrent IPSPs evoked by recurrent activation of interneurons through glutamate stimulation of pyramidal cells in stratum pyramidale (PYR). In response to repetitive electrical stimulation, the peak amplitude of both the O/A glut-IPSP and the PYR glut-IPSP was attenuated (n = 5) in parallel to the reduction in amplitude of the early and late components of the electrically evoked response (stimulus-evoked disinhibition). This suggested the involvement of GABAergic receptors and attested that the interneurons activated during glut-IPSPs were also involved in the circuitry of the electrically evoked IPSPs. The local application of the selective GABAA antagonist bicuculline (100-200 microM) to the slice resulted in a significant reduction in the amplitude of both the O/A (by 76.5%; n = 9) and PYR (by 86.2%; n = 5) glut-IPSPs, in parallel to a decrease of the electrically evoked early IPSP, but not of the late IPSP. The presence of the GABAB antagonist 2-hydroxy-saclofen (1 mM) was able to significantly reduce the amplitude of the O/A glut-IPSPs (by 27.5%; n = 7) and of the electrically evoked late IPSP, but not the PYR glut-IPSP (n = 3). Although the application of phaclofen (20 mM) to the slice reduced the amplitude of the O/A glut-IPSPs (n = 3), the reduction was not statistically significant. These results suggest that recurrent IPSPs elicited from activation of interneurons by stimulation of pyramidal cells are mediated solely via GABAA receptors. Inhibitory postsynaptic potentials elicited from stimulation of interneurons in O/A were also mediated mostly by GABAA receptors, but in addition, displayed a minor component mediated by GABAB receptors. Therefore, since a large proportion of interneurons in O/A are recurrently excited by pyramidal cells (Lacaille J-C et al., 1987, J Neurosci 7: 1979-1993), and since recurrent IPSPs appeared mediated by GABAA receptors, a subpopulation of interneurons activated from O/A might exist that do not receive recurrent excitation but can inhibit pyramidal cells via GABAB receptors.

Animals↗
PubMed1992

Synaptic potentials produced in jaw-closer and jaw-opener motoneurons by palatal stimulation.

Excitation and inhibition of temporal and digastric motoneurons (Temp. and Dig. Mns) during transient jaw closing, the so-called jaw-closing reflex, were studied in cats. Application of diffuse pressure stimulation to the posterior palatal surface produced the jaw-closing reflex and it was found that mechanosensory inputs from the posterior palatal mucosa produce depolarizing potentials on the Temp. Mns responsible for jaw closure during the jaw-closing reflex. We have demonstrated that in one-third of 27 explored Temp. Mns the initial bursts of spikes were elicited before the onset of jaw closure, suggesting that these cells contribute to initiate jaw closure during the jaw-closing reflex. The remaining cells probably contributed to maintain the occlusal phase. Furthermore, it was found that mechanosensory inputs from the posterior palatal mucosa produce a hyperpolarization-depolarization sequence in the Dig. Mns responsible for the jaw-closing reflex. In addition, when pressure stimulation was applied to the anterior palatal mucosa, sustained jaw opening was elicited and an increase of firing frequency of Dig. Mns occurred 40 ms before the onset of jaw opening and continued for 80 ms.

Animals↗
PubMed1982

Formation of functional synapses in the adult cat red nucleus from the cerebrum following cross-innervating of forelimb flexor and extensor nerves. I. Appearance of new synaptic potentials.

We investigated the effects of cross-innervating the peripheral forelimb flexor and extensor nerves of adult cats on the time course of corticorubral EPSPs. Red nucleus neurons were identified by antidromic invasion from C1 or L1 spinal segments as innervating the upper spinal segments (C-cells) or sending axons to the lumbosacral cord (L-cells). In C-cells, a fast-rising component, superimposed on the slow-rising corticorubral EPSPs induced by the cerebral sensorimotor cortex or the cerebral peduncle (CP) stimulation, was noted. The mean time-to-peak of this component in cross-innervated cats operated more than two months earlier was 1.9 +/- 0.9 ms (n = 160), shorter than in normal cats (3.6 +/- 1.4 ms, n = 100). The same value in cats cross-innervated less than two months before was 2.7 +/- 1.0 ms (n = 53). The mean time-to-peak of CP-EPSPs from L-cells was 2.9 +/- 0.9 ms (n = 115). The fast-rising component had a latency of 0.96 +/- 0.19 ms (n = 122), and it was mediated by fibers with conduction velocities of less than 20 m/s. The projective area of the fast-rising component is organized somatotopically. Since it is more sensitive to membrane hyperpolarization than slow rising corticorubral EPSPs, it is mediated by synapses located more proximally than the corticorubral synapses of normal cats. The time course of facilitation by preceding cerebral peduncle stimulation of the nucleus interpositus (IP)-induced RN population responses was measured. It was characterized by a rapid, followed by a slower, rise time in the RN region where C-cells are concentrated. In contrast, the L-cell region was characterized by a slow rise time. In cats subjected to self-union of the peripheral flexor and extensor nerves, the majority of C-cells had CP-EPSPs with a time-to-peak within the normal range. Our results suggest that after cross-innervation sprouting and formation of functional synapses occur on the proximal portion of the soma-dendritic membrane of red nucleus neurons.

Animals↗