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PubMed1997

2-Deoxy-D-glucose-induced changes in membrane potential, input resistance, and excitatory postsynaptic potentials of CA1 hippocampal neurons.

Temporary block of glycolysis by 2-deoxy-D-glucose (2-DG) reversibly suppresses synaptic transmission in the CA1 region of hippocampal slices. Recovery of responses is followed by a sustained potentiation of field excitatory postsynaptic potentials (EPSPs) (2-DG-LTP). To investigate the mechanisms involved in this type of LTP, we studied the effects of 2-DG on membrane properties of CA1 neurons (in slices from Sprague-Dawley rats), recorded with sharp intracellular electrodes containing 3 M KCl, as well as patch electrodes, filled mainly with 150 mM KMeSO4 and Hepes. The predominant change produced by 15- to 20-min applications of 2-DG (10 mM, replacing glucose) was hyperpolarization (-5.6 +/- 1.1 mV for 18 intracellular recordings and -7.2 +/- 0.80 mV for 17 whole-cell recordings) accompanied by a fall in resistance (-33 +/- 2.5% for 14 intracellular recordings and -11.6 +/- 7.1% for 15 whole-cell recordings). Virtually identical hyperpolarizations were recorded in the presence of 20 microM glyburide (-5.5 +/- 1.5 mV, n = 6), but they were abolished by adenosine antagonists 8-(p-sulfophenyl)theophylline (8-SPT) and 8-cyclopentyl-3,7-dihydro-1,3-dipropyl-1H-purine-2,6-dione (DPCPX) (2.8 +/- 1.6 and 4.0 +/- 1.7 mV, respectively; n = 5 for both). It was concluded that the hyperpolarization is most likely caused by an increase in K+ conductance, activated by a 2-DG-induced rise in adenosine release. After such applications of 2-DG, a sustained potentiation of EPSPs (similar to the 2-DG-LTP of field EPSPs) was evident in five neurons recorded with intracellular electrodes but not in any of nine whole-cell recordings, where it was replaced by sustained, LTD-like depression. We conclude that a factor essential for 2-DG-LTP induction is lost during whole-cell recording.

Animals↗

PubMed1993

Characterization of cholinergic and noradrenergic slow excitatory postsynaptic potentials from rat cerebral cortical neurons.

Intracellular recordings from layer V pyramidal neurons in rat somatosensory neocortical slices were used to investigate the effects of electrically stimulating slices known to contain cholinergic and noradrenergic fibers. Repetitive electrical stimulation ventral to the recording site elicited a series of fast excitatory postsynaptic potentials followed by an inhibitory postsynaptic potential. These potentials were followed by a slow excitatory postsynaptic potential that lasted up to tens of seconds. The slow excitatory postsynaptic potential was more prominent when neurons were depolarized to 5-10 mV below firing threshold and was associated with increased input resistance and generated action potentials. The slow excitatory postsynaptic potential increased the amplitude of membrane potential oscillations and blocked the slow afterhyperpolarization which followed trains of action potentials. The amplitude of the slow excitatory postsynaptic potential was sensitive to extracellular potassium concentration. Blockade of postsynaptic action potentials by QX-314 did not block slow excitatory postsynaptic potentials. Exposure of slices to tetrodotoxin did block slow excitatory postsynaptic potentials, indicating they were dependent on propagated action potentials. Application of antagonists of glutamate and fast GABA responses failed to block slow excitatory postsynaptic potentials. Exposure to atropine or either propranolol or atenolol partially antagonized slow excitatory postsynaptic potentials, but only when atropine was added in combination with one of the other agents was the slow excitatory postsynaptic potential completely blocked. Exposure of slices to eserine, imipramine, or cocaine enhanced slow excitatory postsynaptic potentials. It is concluded that the slow excitatory postsynaptic potential triggered in neocortical slices is a composite of a cholinergic and a noradrenergic slow excitatory postsynaptic potential, and these potentials are capable of altering the firing properties of neurons for tens of seconds.

Acetylcholine↗

PubMed1990

Changes in field excitatory postsynaptic potential shape induced by tetanization in the CA1 region of the guinea-pig hippocampal slice.

The present paper contains a description of a prolonged potentiation of the field excitatory postsynaptic potential in the CA1 region of the hippocampal slice preparation following afferent tetanization. In contrast to long-term potentiation, this novel potentiation is not specific to the activated synapses, and manifests itself as a change in the shape of the field excitatory postsynaptic potential with a prolongation of the rising phase and an increased peak amplitude. The potentiation is fully developed within minutes after tetanization and shows no decrement for at least an hour. Although it can appear together with long-term potentiation following tetanization at moderate strength (single volley excitatory postsynaptic potential below threshold for spike initiation), it is more readily seen following tetanization at higher strengths. The N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonovalerate prevents the induction but not the maintenance of the shape modification. The potentiation is observed in the presence of the GABAA antagonist picrotoxin (100 microM) and is thus not secondary to changes in postsynaptic inhibition. 4-Aminopyridine (50-100 microM) produced changes in the field excitatory postsynaptic potential resembling the shape modification produced by afferent tetanization, suggesting that the potentiation may be due to a blockade of potassium channels, pre- or postsynaptically located. The potentiation is also found to be associated with an increase in the population spike for a given initial slope of the field excitatory postsynaptic potential, and may thus contribute to the excitatory postsynaptic potential-spike potentiation that can be observed following afferent tetanization.

2-Amino-5-phosphonovalerate↗

PubMed2004

Dual effect of GABA on descending monosynaptic excitatory postsynaptic potential in frog lumbar motoneurons.

Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by stimulating ipsilateral ventrolateral column (VLC) in the thoracic section were recorded in lumbar motoneurons within the isolated spinal cord of the frog Rana ridibunda. Bath application of the selective GABAB receptor agonist (-)-baclofen (0.05 mM) caused a reduction in the peak amplitude of VLC EPSP. Baclofen did not cause any consistent change in the membrane potential or in the EPSP waveform within frog motoneurones. The selective GABA(B) receptor antagonist saclofen (0.1 mM) completely blocked the effect of (-)-baclofen on VLC EPSP. A decrease in VLC EPSP peak amplitude was also observed during GABA (0.5 mM) application. Unlike (-)-baclofen, inhibition of VLC EPSP induced by GABA was accompanied by a shortening of the EPSP time course and a reduction in membrane input resistance within lumbar motoneurons. The decrease in VLC EPSP peak amplitude induced by (-)-baclofen and GABA was accompanied by an increase in the paired-pulse facilitation. These data provide evidence for a dual pre- and postsynaptic GABAergic inhibition of the VLC monosynaptic EPSP in lumbar motoneurons within the frog spinal cord.

Animals↗

PubMed1993

Fluctuations in pyramid-pyramid excitatory postsynaptic potentials modified by presynaptic firing pattern and postsynaptic membrane potential using paired intracellular recordings in rat neocortex.

Single axon excitatory connections between pairs of neocortical pyramidal neurons were studied using paired intracellular recordings in layers II/III and IV of coronal slices of adult rat somatosensory/motor cortex. Excitatory postsynaptic potentials evoked with different presynaptic firing patterns and at different postsynaptic membrane potentials were compared. Two methods of statistical analysis were used in attempts to determine whether changes in mean excitatory postsynaptic potential amplitude were due to presynaptic or postsynaptic modifications. Analysis of the decrease in mean excitatory postsynaptic potential amplitude associated with increases in presynaptic firing rate were consistent with a change in probability of transmitter release. Paired pulse depression appeared to exhibit both presynaptic and postsynaptic components when the interspike interval was < 10 ms, but could be explained simply by a decrease in probability of release with interspike intervals between 10 and 80 ms. Previous studies had demonstrated that these excitatory postsynaptic potentials are partially mediated by N-methyl-D-aspartate receptors. In contrast to the apparently presynaptic effects of firing pattern, postsynaptic membrane depolarization appeared to produce an increase in quantal amplitude. In addition to this increase at low frequencies, a form of frequency-dependent, self-potentiation involving the recruitment of an additional, longer-latency postsynaptic component occurred at higher presynaptic firing rates. The possibility is discussed that two different mechanisms are involved in the replacement of vesicles at release sites. Over a few tens of milliseconds (paired-pulse depression) availability of releasable transmitter may be determined by the rate of replacement of discharged vesicles from a readily releasable pool of vesicles. Over longer periods of firing at 0.33-2 Hz, the readily releasable pool may become exhausted and require replenishment. Postsynaptic depolarization increases the duration of these excitatory postsynaptic potentials, facilitating summation and enables two components of excitatory postsynaptic potential enhancement at N-methyl-D-aspartate receptor-mediated synapses; one that is present at all firing rates and relates simply to voltage dependent events and one that occurs at higher firing rates and involves a gradual, time dependent event. These data also indicate that the optimal pyramidal firing pattern if another pyramid is to be activated is a tonic, or brief burst pattern at relatively low repetition rates. Long bursts of many presynaptic spikes recruit little that is not activated by pairs of spikes. This situation is in stark contrast to the results obtained in the following paper in which excitatory inputs from pyramids to non-pyramids are described.

Animals↗

PubMed1983

Modulation of action potential during the late slow excitatory postsynaptic potential in bullfrog sympathetic ganglia.

The spike peak and after-hyperpolarization of the action potential of bullfrog sympathetic ganglion cells were depressed during the late slow excitatory postsynaptic potential (EPSP). These changes in the action potential were mimicked by luteinizing hormone-releasing hormone (LH-RH), a neurotransmitter candidate for the late slow EPSP. LH-RH (5 microM) suppressed the voltage-dependent K+ currents, both the delayed rectifier K+ current (IK1) and the M current (IK2). It is suggested that the depression of the after-hyperpolarization of the action potential during the late slow EPSP may be due to suppression of IK1 and IK2.

Action Potentials↗

PubMed1993

Somatostatin regulates excitatory amino acid receptor-mediated fast excitatory postsynaptic potential components in vagal motoneurons.

Somatostatin is considered to be a brain neurotransmitter/neuromodulator; however, there is little concrete information on how this peptide contributes to generation of synaptic potentials in the mammalian central nervous tissue. Recently, a well-defined somatostatin-containing pathway has been traced from the subnucleus centralis of the solitarial complex to the compact formation of the nucleus ambiguus. Moreover, we have demonstrated both in vivo and in vitro that somatostatin enhances glutamate but inhibits acetylcholine excitation of ambigual motoneurons, suggesting involvement of this peptide in central oesophagomotor transmission. The availability of a brainstem slice containing this pathway has allowed us to characterize an excitatory amino acid receptor-mediated excitatory postsynaptic potential in compact formation neurons. This excitatory postsynaptic potential is unusual because its rising phase involves activation of N-methyl-D-aspartate receptors. Here we report that somatostatin participates in ambigual excitatory postsynaptic potential generation by permitting expression of the N-methyl-D-aspartate receptor-mediated component, thereby regulating fast information transfer in this pathway.

Animals↗

PubMed1992

Fast excitatory postsynaptic potentials and the responses to excitant amino acids of sympathetic preganglionic neurons in the slice of the cat spinal cord.

The properties of the excitatory postsynaptic potential evoked by focal stimulation and of the responses to excitatory amino acids were examined by intracellular recording from sympathetic preganglionic neurons in upper thoracic spinal cord slices of the adult cat. Single stimuli to the region dorsal to the intermedio-lateral nucleus evoked short-latency, presumably monosynaptic, excitatory postsynaptic potentials. The reversal potential of this response was -2.2 mV and became more negative when external Na+ or K+ concentration was decreased. The excitatory postsynaptic potential was depressed by the non-selective excitatory amino acid receptor antagonist cis-2,3-piperidine dicarboxylic acid and enhanced by a glutamate uptake inhibitor. The non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2.3-dione abolished the excitatory postsynaptic potential in 72% of neurons. In the remaining neurons, this antagonist only depressed the potential and unmasked a slower component which was abolished by the N-methyl-D-aspartate receptor antagonist D,L-2-amino-5-phosphonovaleric acid. In the presence of tetrodotoxin all neurons tested were depolarized by glutamate or aspartate, as well as by the selective agonists quisqualate, alpha-amino-3-hydroxy-5-methylisoxazole propionic acid, kainate and N-methyl-D-aspartate. The glutamate-evoked depolarization reversed at a membrane potential of -2.0 mV and at a more negative value when external Na+ or K+ concentration was decreased. The response to alpha-amino-3-hydroxy-5-methylisoxazole propionic acid was abolished by 6-cyano-7-nitroquinoxaline-2,3-dione in all neurons tested and that to kainate in only one-third of the cells. In the remainder the response to kainate was only slightly depressed by this antagonist. The responses to glutamate and aspartate were only slightly depressed by the combined action of the various amino acid receptor antagonists used. The responses to N-methyl-D-aspartate were abolished by D,L-2-amino-5-phosphonovaleric acid. The punched-out region of the intermedio-lateral nucleus, maintained in vitro, released glutamate and aspartate in the absence of stimulation. Field stimulation (20 Hz) enhanced release by between 40 and 100%. The increase was prevented by superfusion with calcium-free Krebs. It is concluded that excitatory amino acids, acting on both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors, but mainly on the latter, are likely mediators of the monosynaptic excitatory postsynaptic potential evoked in sympathetic preganglionic neurons by the stimulated region. The efflux data suggest that glutamate and aspartate are among the mediators.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMedDate not supplied

Hyperpolarization following activation of K+ channels by excitatory postsynaptic potentials.

We have postulated that an excitatory postsynaptic potential (e.p.s.p.) may open voltage-sensitive K+ ('M') channels, in an appropriate depolarizing range, and that this could alter the e.p.s.p. waveform. Consequently, the fast e.p.s.p. in neurones of sympathetic ganglia, elicited by a nicotinic action of acetylcholine (ACh), could be followed by a hyperpolarization, produced by the opening of M channels during the depolarizing e.p.s.p. and their subsequent slow closure (time constant-150 mg). This introduces the concept that transmitter-induced p.s.ps may trigger voltage-sensitive conductances other than those initiating action potentials, and that in the present case this could produce a true post-e.p.s.p. hyperpolarization. (Some hyperpolarizations other than inhibitory postsynaptic potentials (i.p.s.ps) have been reported to follow e.p.s.ps.) We show here that this is so.

Animals↗

PubMed1993

Single axon excitatory postsynaptic potentials in neocortical interneurons exhibit pronounced paired pulse facilitation.

In slices of adult rat somatosensory/motor cortex, paired recordings were made from pyramidal and non-pyramidal neurons. Single axon excitatory postsynaptic potentials evoked in the non-pyramidal neuron by action potentials in the pyramidal neuron were large and fast and demonstrated large fluctuations in amplitude, with coefficients of variation between 0.1 and 1.25. Excitatory postsynaptic potential amplitude distributions included a large number of apparent failures of transmission as well as some extremely large events. This contrasted dramatically with the relatively narrow distribution of amplitudes for pyramid-pyramid connections in neocortex. Excitatory postsynaptic potentials increased in amplitude with postsynaptic membrane hyperpolarization. Very small changes in the coefficient of variation when mean amplitudes increased substantially were consistent with the increase being due to a change in quantal amplitude. These excitatory postsynaptic potentials displayed profound paired pulse facilitation. Moreover, third and fourth spikes in a presynaptic burst also evoked large responses. This facilitation was associated with a decrease in the proportion of apparent failures in transmission and a change in the shape of the excitatory postsynaptic potential amplitude distribution, both indicative of an increase in the probability of transmitter release. However a large change in the mean amplitude was not associated with a similar change in the inverse square of the coefficient of variation. The result of this third test, taken in isolation, might therefore suggest that quantal amplitude had increased with paired-pulse facilitation. However, of the three tests applied, this last is the most heavily model-dependent and produced a result inconsistent with the results of the other two tests. The possibility is therefore discussed that both the shape of the excitatory postsynaptic potential amplitude distribution and the failure of coefficient of variation analysis to detect an apparently presynaptic change might result from the release at these synapses being poorly fit by a simple model. Based on a more complex model of synaptic release proposed by Faber and Korn [Faber and Korn (1991) Biophys. J. 60, 1288-1294] and a hypothesis proposed by Scharfman et al. [Scharfman et al. (1990) Neuroscience 37, 693-707], two hypotheses arising from the present study are discussed: (i) that branch point failure contributes to the pattern of synaptic activation at these connections; and (ii) that both presynaptic pyramidal firing pattern and axonal geometry contribute to the selection of the type of postsynaptic neurone preferentially activated.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1999

Dynamic properties of corticothalamic excitatory postsynaptic potentials and thalamic reticular inhibitory postsynaptic potentials in thalamocortical neurons of the guinea-pig dorsal lateral geniculate nucleus.

The properties of postsynaptic potentials evoked by stimulation of cortical, retinal and GABAergic thalamic afferents were examined in vitro in thalamocortical neurons of the guinea-pig dorsal lateral geniculate nucleus. Brief trains of stimulation (2-10 stimuli) delivered to corticothalamic fibers led to a frequency-dependent increase in excitatory postsynaptic potential amplitude associated with an increase in activation of both N-methyl-D-aspartate and non-N-methyl-D-aspartate glutamate receptors. In addition, repetitive stimulation of corticothalamic fibers also gave rise to a slow excitatory postsynaptic potential that was blocked by local application of the glutamate metabotropic receptor antagonist alpha-methyl-4-carboxyphenylglycine. In contrast, repetitive stimulation of optic tract fibers resulted in monosynaptic excitatory postsynaptic potentials that did not potentiate and were not followed by the generation of a slow excitatory postsynaptic potential. Repetitive activation of the optic radiation also evoked both GABA(A) and GABA(B) receptor-mediated inhibitory postsynaptic potentials. These inhibitory postsynaptic potentials exhibited frequency-dependent depression during repetitive activation. The presence of frequency-dependent facilitation of corticothalamic excitatory postsynaptic potentials and frequency-dependent decrement of inhibitory postsynaptic potentials, as well as the ability of corticothalamic fibers to activate glutamate metabotropic receptors, suggests that sustained activation of corticothalamic afferents in vivo may result in postsynaptic responses in thalamocortical cells that are initially dominated by GABAergic inhibitory postsynaptic potentials followed by prominent monosynaptic excitatory postsynaptic potentials as well as a slow depolarization of the membrane potential.Therefore, the corticothalamic system may inhibit or enhance the excitability and responsiveness of thalamocortical neurons, based both on the spatial and temporal features of thalamocortical interactions.

Animals↗

PubMed1995

Properties of single axon excitatory postsynaptic potentials elicited in spiny interneurons by action potentials in pyramidal neurons in slices of rat neocortex.

In slices of adult rat somatomotor cortex, paired intracellular recordings determined the properties of a novel class of excitatory connection, that of presynaptic pyramidal axon collaterals onto burst firing, spiny inhibitory interneurons. Single axon excitatory postsynaptic potentials were brief in time course and displayed conventional voltage relations, increasing in amplitude with membrane hyperpolarization with no change in time course. Excitatory postsynaptic potential amplitude distributions were not skewed. Paired pulse facilitation was profound at interspike intervals < 50 ms, but not altered by raising extracellular [Ca2+] from 2.5 to 5 mM, despite an apparent increase in release probability. Raising presynaptic firing frequency did however produce an increase in excitatory postsynaptic potentials elicited by first spikes that was associated with a decline in excitatory postsynaptic potentials elicited by second and third spikes in brief trains of presynaptic spikes. That this pattern of synaptic activity may result from low probabilities of transmitter release is discussed. It is proposed that while raising Ca2+ and increasing presynaptic firing both increase release probability, repetitive presynaptic firing raises probability more effectively than does raising extracellular [Ca2+]. However, concomitant exhaustion of readily releasable transmitter at higher firing rates may partially obscure this effect. It is concluded that the major differences in the firing rate- and firing pattern-dependent properties of pyramid-pyramid and pyramid-interneuron connections are due to the typically lower release probability at synapses onto interneurons. The accompanying paper describes the morphology of these connections.

Action Potentials↗

PubMed2001

Excitatory postsynaptic potentials trigger a plateau potential in rat subthalamic neurons at hyperpolarized states.

The subthalamic nucleus (STN) directly innervates the output structures of the basal ganglia, playing a key role in basal ganglia function. It is therefore important to understand the regulatory mechanisms for the activity of STN neurons. In the present study, we aimed to investigate how the intrinsic membrane properties of STN neurons interact with their synaptic inputs, focusing on their generation and the properties of the long-lasting, plateau potential. Whole cell recordings were obtained from STN neurons in slices prepared from postnatal day 14 (P14) to P20 rats. We found that activation of glutamate receptor-mediated excitatory synaptic potentials (EPSPs) evoked a plateau potential in a subpopulation of STN neurons (n = 13/22), in a voltage-dependent manner. Plateau potentials could be induced only when the cell was hyperpolarized to more negative than about -75 mV. Plateau potentials, evoked with a depolarizing current pulse, again only from a hyperpolarized state, were observed in about half of STN neurons tested (n = 162/327). Only in neurons in which a plateau potential could be evoked by current injection did EPSPs evoke plateau potentials. L-type Ca(2+) channels, Ca(2+)-dependent K(+) channels, and TEA-sensitive K(+) channels were found to be involved in the generation of the potential. The stability of the plateau potential, tested by the injection of a negative pulse current during the plateau phase, was found to be robust at the early phase of the potential, but decreased toward the end. As a result the early part of the plateau potential was resistant to membrane potential perturbations and would be able to support a train of action potentials. We conclude that excitatory postsynaptic potentials, evoked in a subpopulation of STN neurons at a hyperpolarized state, activate L-type Ca(2+) and other channels, leading to the generation of a plateau potential. Thus about half of STN neurons can transform short-lasting synaptic excitation into a long train of output spikes by voltage-dependent generation of a plateau potential.

2-Amino-5-phosphonovalerate↗

PubMed1983

Summation of excitatory postsynaptic potentials in hippocampal pyramidal cells.

The summation of excitatory postsynaptic potentials (EPSPs) generated in separate parts of the dendritic tree of hippocampal pyramidal cells has been investigated using the in vitro slice preparation. Two separate inputs with known synaptic location were used. The EPSP produced by simultaneous activation of the two inputs (observed sum) was compared to the algebraic sum of the individual EPSPs. Small-amplitude EPSPs (0.5-1.5 mV) added linearly. The shortest distance between the two synaptic groups was 75 micron. With larger amplitudes (greater than 2.5 mV), the EPSP summated nonlinearly. The nonlinear summation was reduced by moderate hyperpolarizations (2-10 mV) of the soma membrane. Also, large EPSPs (greater than 2.5 mV) summated linearly when the peak of the summed EPSP was brought close to the equilibrium potential for the inhibitory postsynaptic potential (IPSP) (EIPSP). When the EPSP peak was made more negative than the EIPSP, summation was again nonlinear but the algebraic sum was now smaller than the observed EPSP sum, i.e., the direction of the nonlinearity was reversed. EPSP summation was linear after the IPSP had been blocked by benzyl penicillin application. We conclude that separate EPSPs in hippocampal pyramids (minimal separation, 75 micron) add linearly but that the addition of an IPSP may complicate this picture. No evidence was found for interaction between the different populations of excitatory synapses.

Animals↗

PubMedDate not supplied

Reciprocal inhibition of the AMPA and NMDA components of excitatory postsynaptic potentials in field CA1 of the rat hippocampus in vitro.

The mutual effects of components of excitatory postsynaptic potentials (EPSP) induced by activation of glutamate receptors sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) were studied on living slices of rat hippocampus. Evoked responses were recorded in the radial layer (stratum radialis) in field CA1 after stimulation of collateral-commissural fibers. The contribution of the NMDA component to the total EPSP was altered by extracellular application of solutions containing different concentrations of magnesium. At low magnesium concentrations, when both components made significant contributions to EPSP, inhibition of one of the components by application of antagonists of the appropriate receptors led to increases in the area of the other component. Thus, the total magnitude of pharmacologically isolated components were significantly greater than the control response (for example, at 0.1 mM magnesium, the sum of the components was 340 +/- 120% of the control two-component EPSP (p < 0.01; N = 6). These results suggest that in controls, the AMPA and NMDA components of EPSP inhibit each other. The mutual inhibition of components may be an important factor affecting the conductivity and plastic properties of central glutamatergic synaptic pathways.

Animals↗

PubMed1988

Voltage-clamp analysis of taurine-induced suppression of excitatory postsynaptic potentials in frog spinal motoneurons.

1. The depressant actions of taurine applications on lumbar motoneurons in the isolated frog spinal cord were studied using conventional intracellular recordings and the two-electrode voltage-clamp technique. 2. With microelectrodes containing K+-acetate, 0.75-2 mM taurine mostly induced a hyperpolarization that often faded or turned into depolarization during the continuous application. A higher concentration (5-7.5 mM) depolarized a majority of cells. The effects on the membrane potential were associated with an increase in input conductance (approximately 285%). 3. The reversal potential of the taurine-induced currents was approximately -70 mV, with microelectrodes containing K+-acetate. In recordings using KCl-filled electrodes, taurine (less than or equal to 2 mM) produced a large depolarization (greater than or equal to 20 mV) at resting potentials near -50 mV, thereby indicating that the reversal potential was positively shifted by loading the cell with Cl-. These results suggest that the taurine potentials were mediated predominantly by an increased Cl- permeability. 4. Voltage-dependent relaxations of taurine currents were observed in 10 of 14 neurons. 5. A linear relation was found between the input conductance and the amount of current required to generate a 1-mV increment in EPSP at resting potential. 6. Polysynaptic excitatory postsynaptic potentials (EPSPs) and currents (EPSCs) were more susceptible to taurine than the monosynaptic responses. Taurine (less than 1 mM) seemed to suppress the interneurons mediating polysynaptic pathways. 7. Monosynaptic EPSPs and EPSCs were decreased with higher concentrations of taurine (greater than 1 mM). The percent reduction of EPSPs and that of the corresponding EPSCs had a positive correlation (r = 0.95), whereas, there was no significant correlation between changes in EPSPs and in input conductance, and between changes in EPSCs and in input conductance. The amount of current required to produce a 1-mV increment of EPSP was increased in the presence of taurine, in association with the increased input conductance. 8. Taurine suppressed synaptic potentiation of EPSPs evoked by paired stimuli, at an interval of 60-180 ms. Gamma-D-glutamylglycine, an antagonist of receptors for excitatory amino acids, greatly reduced the amplitude of EPSPs, but had little effect on synaptic potentiation. 9. Taurine suppressed glutamate currents evoked at membrane potentials, clamped near rest in low Ca2+, high Mg2+ solution. 10. These findings suggest that the taurine-induced reduction of EPSPs is due mainly to suppression of EPSCs, through both presynaptic and postsynaptic mechanisms.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Voltage dependence of excitatory postsynaptic potentials of rat neocortical neurons.

1. The properties of excitatory postsynaptic potentials (EPSPs) of rat neocortical neurons were investigated with a fast single-electrode current-voltage clamp in vitro. Typically, apparently pure EPSPs were obtained by selection of electric stimuli of low intensity. 2. The amplitude and time integral of the EPSP increased when the neuron was depolarized. At threshold for generation of action potentials, the amplitude of EPSPs was increased by approximately 30% [from 5.0 +/- 2.1 to 6.3 +/- 1.0 (SD) mV, n = 12]. The integral of EPSPs was maximally about fourfold (3.7 +/- 1.5, n = 16) larger than at resting membrane potential (Em). The mechanisms involved in this augmentation of EPSPs were further investigated. 3. The amplitude and the time integral of excitatory postsynaptic currents (EPSCs) decreased linearly with shifts in command potential from -100 to -60 mV. The decrease of the EPSC integral with depolarization indicates that the enhancement of the EPSP may be brought about by recruitment of a voltage-dependent inward current. 4. Evoking EPSPs at various delays after the onset of small depolarizing current pulses (0.3-0.6 nA, 600 ms) revealed that augmentation decays with time. The integral of EPSPs evoked approximately 80 ms after the onset of the current pulse was 3.7 (+/- 1.5, n = 16) times larger than at Em. The integral of EPSPs evoked at 480 ms. however, were only twofold (+/- 0.7, n = 16) larger. Hence EPSPs evoked after a delay of 80 ms were 1.7-fold (+/- 0.4, n = 24) larger than EPSPs evoked after 480 ms. EPSCs were independent of the delay of stimulation at all potentials. 5. Intracellular application of the lidocaine derivative N-(2,6-dimethyl-phenylcarbamoylmethyl) triethylammonium bromide (QX 314) at 100 mM from pipettes rapidly abolished fast action potentials and inward rectification. During comparable depolarizations the increase in EPSP integrals was much smaller in QX 314-treated neurons than in controls. On average, the integral of EPSPs evoked at 70-90 ms was 1.7 times (+/- 1.0) larger than at Em, and the integral of EPSPs evoked with larger delays was close to the value obtained at resting Em (0.9 +/- 0.3, n = 8). The ratio of EPSP integrals early versus late (1.8 +/- 0.5) is comparable to controls, suggesting that QX 314-sensitive currents are unlikely to be involved in the time-dependent enhancement. 6. Mimicking EPSPs by brief depolarizations atop long depolarizations revealed a time- and voltage-dependent enhancement comparable to that of EPSPs.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1973

Pentobarbital: selective depression of excitatory postsynaptic potentials.

The effects of pentobarbital (Nembutal) on synaptic transmission and postsynaptic potentials were studied by the use of several invertebrate preparations. Pentobarbital selectively and reversibly depressed both excitatory postsynaptic potentials and sodium-dependent postsynaptic responses to putative excitatory transmitters without affecting either inhibitory postsynaptic potentials or chloride- and potassium-dependent postsynaptic responses to putative transmitters. A selective depression of postsynaptic excitatory events was also observed with other central nervous system depressants (ethanol, chloroform, chloralose, diphenylhydantoin, and urethane). The results suggest that central and peripheral depression observed during general anesthesia is due to a selective depression of excitatory synaptic events.

Acetylcholine↗