SEARCH · PubMed Health

Results for “Inhibitory Postsynaptic Potentials”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 577 records · Page 32Linked to original sources

PubMed1980

Potentiation of excitatory postsynaptic potentials during and after repetitive stimulation in thin hippocampal sections.

Excitatory postsynaptic potentials (EPSPs) elicited by mossy fiber stimulation were recorded intracellularly from neurons in the CA3 region in thin hippocampal sections in vitro and potentiation of the EPSPs was examined during and after repetitive stimulation. Inhibitory postsynaptic potentials (IPSPs) and seizure discharges were blocked by bicuculline and high concentrations of Mg2+. When two shocks were applied at short intervals, the second EPSP was markedly potentiated. This potentiation declined exponentially with a time-constant of about 180 ms and was unaffected by changes in ambient temperature. The amount of potentiation during a pulse train was explained by summation of potentiation by individual pulses. Post tetanic potentiation lasted longer in media containing Ca2+ at higher concentrations and Mg2+ at lower concentrations. At high Ca2+ concentrations, tetanic stimulation induced long-term potentiation which was occasionally preceded by a long-lasting suppression. Tetanus to a bundle of mossy fibers potentiated EPSPs elicited by stimulation of a separate bundle of mossy fibers (heterosynaptic potentiation) but did not augment EPSPs elicited by fimbrial stimulation.

Animals↗

PubMed1992

Sustained and selective block of IPSPs in brain slices from rats made epileptic by intrahippocampal tetanus toxin.

A small dose of tetanus toxin (2-5 ng; 10 mouse LD50) injected into the rat hippocampus produces a chronic epileptic syndrome in which epileptic discharges recur intermittently for 6-8 weeks. Hippocampal slices prepared during this period and maintained in vitro generate both evoked and spontaneous epileptic discharges. The present study used slices prepared 8-18 days after injection of tetanus toxin or vehicle solution into both hippocampi to test whether or not synaptic inhibition was selectively impaired in this experimental epilepsy. Intracellular recordings were made from CA3 pyramidal layer neurones within the tetanus toxin focus, which was identified by field potential recordings of synchronous bursts evoked by afferent stimulation. The intrinsic properties of these neurones did not differ from comparable cells in control-injected rats. All cells generated excitatory postsynaptic potentials (EPSPs) following stimulation of stratum radiatum in CA3. In control slices EPSPs were followed by a 'fast' inhibitory postsynaptic potential (IPSP), peaking at 25-30 ms, with a mean amplitude (+/- SEM) of -6.7 mV (+/- 0.66). In the epileptic slices these were absent, and the EPSP prolonged so that the potential at 30 ms was a depolarisation of +6.6 mV (+/- 2.75). The slow IPSP at 120 ms dropped to -0.27 mV (+/- 0.18) from -3.97 mV (+/- 1.43) (11 cells in each group). The loss of IPSPs cannot be attributed to a shift in reversal potentials in the toxin-injected group because no IPSPs were unmasked by current injection (n = 11). IPSPs also occurred spontaneously in the neurones in control slices, with a mean amplitude of -1.30 mV. Their frequency decreased by a factor of 13 in cells from the chronic focus induced by tetanus toxin (P less than 0.0001, analysis of variance), but their amplitude did not change significantly (mean of -1.22 mV). Spontaneous EPSPs were significantly more frequent and slightly smaller in the toxin-injected group (mean amplitudes 1.35 and 1.13 mV respectively). Together these studies support the hypothesis that the chronically recurring seizures induced by low doses of tetanus toxin can be attributed to a substantial, persistent and selective reduction of inhibitory neurotransmission in the hippocampus.

Animals↗

PubMed1994

Hypoxia-activated Ca2+ currents in pacemaker neurones of rat rostral ventrolateral medulla in vitro.

We examined the effects of brief periods of hypoxia or application of cyanide on the discharge and membrane properties of medullary pacemaker neurones in slices of the rostral ventrolateral reticular nucleus (RVL) of the medulla oblongata of rats. Stable intracellular recordings were obtained from seventy-nine neurones within the RVL which exhibited spontaneous rhythmic discharge in the absence of excitatory postsynaptic potentials (EPSPs). The membrane potential cycles of these neurones could be reset with an evoked spike without eliciting EPSPs or inhibitory postsynaptic potentials and hence met criteria of RVL pacemaker neurones. Hypoxia, produced by reducing O2 from 95 to 20% for 40 s or exposure to cyanide (30-300 microM for 40 s), reversibly increased neuronal discharge 1.6-fold (20% O2) or 2.6-fold (300 microM cyanide), respectively, in association with membrane depolarization and a significant fall in membrane resistance. The membrane responses to hypoxia and cyanide were observed in the presence of tetrodotoxin (TTX) at a concentration (10 microM) which eliminated spontaneous spikes or spikes evoked by intracellular depolarization. When recorded at a holding potential of -70 mV by single-electrode voltage clamp, hypoxia or cyanide (300 microM) elicited inward currents of 0.44 +/- 0.06 and 0.58 +/- 0.08 nA, respectively, which are attenuated by reducing the concentration of extracellular Ca2+ ions, and abolished by 2 mM CoCl2 and 100 microM NiCl2, but not affected by 50 microM CdCl2, replacement of 83% extracellular Na+, or adenosine deaminase (2U ml-1). We conclude that hypoxia and cyanide directly excite RVL pacemaker neurones in vitro by a common mechanism: activation of Ca2+ channel conductance.

Action Potentials↗

PubMed1999

Self-sustained rhythmic activity in the thalamic reticular nucleus mediated by depolarizing GABAA receptor potentials.

Intracellular recordings from reticular thalamic (RE) neurons in vivo revealed inhibitory postsynaptic potentials (IPSPs) between RE cells that reversed and became depolarizing at the hyperpolarized membrane potentials that occur during sleep. These excitatory IPSPs can directly trigger low-threshold spikes (LTSs). The oscillatory mechanisms underlying IPSP-triggered LTSs crowned by spike bursts were investigated in models of isolated RE networks. In a one-dimensional network model, external stimulation evoked waves of excitation propagating at a constant velocity of 25-150 cells per second. In a large-scale, two-dimensional model of the reticular nucleus, the network showed transient or self-sustained oscillations controlled by the maximum conductance of the low-threshold calcium current and the membrane potential. This model predicts that the isolated reticular nucleus could initiate sequences of spindle oscillations in thalamocortical networks in vivo.

Action Potentials↗

PubMed1986

Autoradiographic measurement of tritiated agmatine as an indicator of physiologic activity in Hermissenda visual and vestibular neurons.

[3H]Agmatine (amino-4-guanidobutane) has been shown to be potentially useful for identifying and assessing the ACh sensitivity of specific neurons. Small cationic amines are able to permeate ACh-activated ion channels in sympathetic neurons and vertebrate endplates. Sensory neurons of the photic pathway in the nudibranch mollusc Hermissenda crassicornis are cholinergic and the synaptic interactions between the photic and vestibular systems have been well characterized electrophysiologically. We have therefore tested the feasibility of using autoradiography with [3H]agmatine, (a) to identify known ACh-responsive postsynaptic cells and (b) to examine its ability to serve as an indicator of physiologic activity within the photic and vestibular pathways under conditions of darkness and light stimulation. Scintillation counting revealed that approximately 70% of the radioactivity was associated with the CNS while approximately 30% was found in the processing fluids, indicating that routine glutaraldehyde-osmium fixation and subsequent processing for epoxy embedding allows retention of substantial amounts of the radiolabel. The autoradiographic results consistently demonstrated that the uptake patterns for [3H]agmatine did reflect some of the known neuronal interactions under the experimental conditions of light and dark. The accuracy extended to the second order cells of the optic ganglion and to putative interneurons along the photic tract in the cerebropleural ganglion. Since all the neurons in these pathways are unipolar with their synaptic interactions occurring only at the terminal endings, the radiolabel accumulated in the somata resulted from retrograde axonal transport. In the photic-vestibular pathways, the highest silver grain densities were found over structures (cell bodies or axon tracts) with increased synaptic activity coupled with higher levels of cellular activity (i.e. increased excitatory postsynaptic potentials or increased spontaneous impulse activity). Slightly less label was found in cells which received increased numbers of inhibitory postsynaptic potentials that produced hyperpolarization and a transient cessation of impulse activity under conditions of illumination. Therefore, the uptake levels of [3H]agmatine as revealed by autoradiography appear to reflect not only changes in sensitivity or density of ACh-activated channels but also changes in cellular activity as indicated by increased amounts of retrograde transport. These results represent the first example of the effective use of this radiolabel as an indicator of synaptic activity in invertebrates and in sensory systems.

Agmatine↗

PubMed1987

Mechanism of aminopyridine-induced ictal seizure activity in the cat neocortex.

Intracellular recordings were obtained from neurons in the motor cortex of anesthetized cats in order to examine membrane and synaptic processes involved in aminopyridine (AP)-induced ictal seizure activity. Depolarizing and hyperpolarizing membrane potential sequences which behaved as large, synchronized excitatory and inhibitory postsynaptic potentials, were found to accompany the ictal seizure potentials. After several repetitions of the seizure attack, partial responses, bursts and depolarizing plateaus with spike inactivation occurred. In layers IV and V we found non-pyramidal tract neurons showing endogenous bursting ability activated by AP. These neurons seemed to be the initiators of the rhythmic synchronous activity of the epileptic neuron population. Our results suggest that AP-induced epileptogenesis represents an adequate model of ictal events in the neocortex.

Action Potentials↗

PubMed1988

Effects of dithiothreitol, a sulfhydryl reducing agent, on CA1 pyramidal cells of the guinea pig hippocampus in vitro.

The radioprotectant, dithiothreitol (DTT) has been shown to increase excitability in the hippocampal slice preparation. In the present study, intracellular recording techniques were used to further examine the actions of DTT. Electrophysiological recordings from CA1 pyramidal cells were obtained prior to, during and after DTT exposure. DTT caused a small depolarization without altering membrane resistance. DTT induced spontaneous firing and occasional burst firing in normally silent neurons. These effects were accompanied by a reduction in spike frequency adaptation but no change in the afterhyperpolarization following a train of action potentials. Following DTT exposure, orthodromic stimulation produced multiple firing. Subthreshold excitatory postsynaptic potentials (EPSPs) were significantly prolonged. Isolating the CA1 subfield, attenuated the prolongation of the EPSP by DTT. Recurrent inhibitory postsynaptic potentials were unaffected by DTT. The actions of DTT are likely to result from DTT-induced reduction of disulfide bonds since the reduced form of DTT does not cause a similar hyperexcitability.

Action Potentials↗

PubMed1994

Metabotropic glutamate receptor-induced disinhibition is mediated by reduced transmission at excitatory synapses onto interneurons and inhibitory synapses onto pyramidal cells.

Previous studies suggest that activation of metabotropic glutamate receptors (mGluRs) reduces GABA-mediated synaptic inhibition in area CA1 of the hippocampus. However, the mechanisms involved in this disinhibition are not known. We report that mGluR activation reduces both the GABAA and GABAB receptor-mediated components of evoked inhibitory postsynaptic potentials (IPSPs) by reducing transmission at excitatory synapses onto inhibitory interneurons and inhibitory synapses onto CA1 pyramidal cells.

Animals↗

PubMed1994

Responses of CA1 pyramidal neurons in rat hippocampus to transient forebrain ischemia: an in vivo intracellular recording study.

The electrophysiological responses of CA1 pyramidal neurons to 5 min forebrain ischemia were studied with intracellular recording and staining techniques in vivo. The baseline membrane potential rapidly depolarized to approximately -20 mV about 3 min after the onset of ischemia and began to repolarize 1-3 min after recirculation. The amplitude of this ischemic depolarization (ID) was related directly to the severity of ischemia and its latency of onset was inversely related to brain temperature. Spontaneous synaptic activity ceased shortly after ischemia onset while the evoke synaptic potentials lasted until shortly before the onset of ID. Inhibitory postsynaptic potentials (IPSPs) disappeared earlier than excitatory postsynaptic potentials (EPSPs) and the membrane input resistance of CA1 neurons increased after the onset of ischemia.

Action Potentials↗

PubMed1992

PGO-related potentials in lumbar motoneurons during active sleep.

1. The present report describes the relationship that occurs during active sleep between ponto-geniculo-occipital (PGO) waves and changes in spinal cord motoneuron membrane potential. 2. These changes were characterized by the appearance of a complex pattern of motoneuron hyperpolarizing potentials, with a duration of approximately 300 ms, that were centered around the PGO wave. The first hyperpolarizing potential began before the onset of the PGO wave. Emerging from this hyperpolarizing potential was a second, larger-amplitude hyperpolarizing potential; it was followed by a succession of smaller-amplitude hyperpolarizations. 3. All potentials were present in conjunction with PGO waves during active sleep, but they were observed only in some motoneurons when PGO waves occurred during the transition period from quiet sleep to active sleep. 4. The potentials were reversed by chloride, demonstrating that they were inhibitory postsynaptic potentials (IPSPs). 5. These data, combined with the fact that these PGO-related IPSPs are blocked by strychnine, support the hypothesis that they are the result of the phasic enhancement of the activity of the same system that inhibits motoneurons during active sleep.

Action Potentials↗

PubMed1994

Participation of voltage-gated conductances on the response succeeding inhibitory synaptic potentials in the crayfish slowly adapting stretch receptor neuron.

1. We examined the contribution of voltage-gated conductances to inhibitory postsynaptic potential (IPSP) effects under current clamp in silent and spiking slowly adapting stretch receptor neurons (SN1s) in the slow receptor muscle of the crayfish Procambarus. The receptor exemplifies the simplest inhibitory neural circuit, with one presynaptic and one postsynaptic neuron. The effects of synaptic inhibition were compared with the outcome of hyperpolarizing current pulses. Because pulse effects were exclusively due to postsynaptic mechanisms, an estimation of the synaptic or extrasynaptic origin of the results of IPSP was possible. 2. Inhibition by single IPSPs increased gradually with the time elapsed from the preceding spike in 60% of the spiking SN1s. However, early IPSP arrivals were exclusively excitatory in the rest of the cases. Inhibition was restricted to a single expanded SN1 interspike interval, but the early excitation and the postinhibitory rebound lasted several intervals. Rebound was invariably present; it was the only consequence of IPSPs in silent receptors and could be extremely long lasting (> 25 s). 3. The membrane potential of the SN1 neuron was clamped at hyperpolarized values (greater than -65 mV) by prolonged IPSP barrages at high rate (> 20/s). A prominent depolarizing sag and a gradual reduction of the IPSP amplitude were observed with prolonged presynaptic stimulation. There were subthreshold IPSP amplitude oscillations consisting of gradual increases and decreases of the post-IPSP peak depolarization at lower presynaptic rates. IPSP amplitude variations (< or = 10 mV) were primarily due to larger local responses. 4. Essentially all IPSP effects were mimicked by hyperpolarizing pulses. Sag was also evoked by pulses and was accompanied by a gradual conductance increase preceded by a brief initial drop. Sag and rebound were markedly reduced by Cs+ (2 mM) and tetrodotoxin (1 microM) and less by Ba2+ (5 mM) or tetraethylammonium (25 mM) superfusion. Both were somewhat decreased by acetylcholine (30 microM), which also markedly depolarized and accelerated firings, results which were usually reduced by atropine (10 microM). 5. In conclusion, IPSP and hyperpolarizing pulse effects were essentially identical, implying that extrasynaptic membrane properties were decisive. Interestingly, net excitatory consequences were usual, effectively increasing sensitivity and reducing the sensory threshold. Pharmacological evidence is provided suggesting that the hyperpolarization-activated current, IQ, and also probably the K+ M-current, the A-current, and the low-threshold, persistent Na+ conductances participate in sag and rebound genesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Zinc enhances GABAergic transmission in rat neocortical neurons.

1. Intracellular recordings were made in layer II-III neurons of rat neocortical slices maintained in vitro. The effect of bath application of zinc (50-300 microM) on evoked synaptic activity and passive membrane properties was examined. 2. Excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-D-aspartate (NMDA) and non-NMDA receptors were recorded in response to electrical stimulation. Zinc did not affect either type of EPSP. Resting membrane potential, repetitive firing properties, and input resistance were not altered by zinc. 3. Inhibitory postsynaptic potentials (IPSPs) were enhanced after zinc application. Zinc also induced generation of large amplitude spontaneous gamma-aminobutyric acid-A (GABAA)- and GABAB-mediated IPSPs. Postsynaptic responses to iontophoretically applied GABA were unaffected. In the presence of zinc, GABAergic synaptic potentials could result in generation of action potentials. 4. Directly evoked IPSPs recorded in the presence of the excitatory amino acid receptor blockers 6-cyano-7-nitroquinoxaline-2,3-dione and 2-amino-5-phosphonovaleric acid were enhanced by zinc. Under these conditions spontaneous IPSPs with superimposed action potentials were present. Baclofen, in the presence of zinc, reduced the amplitude of evoked IPSPs. 5. These results indicate that zinc may be an endogenously occurring neuromodulator. Zinc appears to enhance GABAergic IPSPs by increasing the excitability of inhibitory interneurons, thus resulting in increased GABA release.

Animals↗

PubMed1994

Electrophysiological and histochemical properties of postnatal rat serotonergic neurons in dissociated cell culture.

Serotonin modulates a variety of neural processes, and is present in a subpopulation of neurons in the raphe nuclei. To study their electrophysiological properties, cells from the mesopontine raphe nuclei of the neonatal rat were dissociated and grown for up to 10 weeks in microcultures. Approximately one third of the neurons were identified as serotonergic based on the presence of serotonin immunoreactivity, tryptophan hydroxylase immunoreactivity, or a high affinity monoamine transporter. About 5% of cultured raphe neurons contained tyrosine hydroxylase immunoreactivity, while 25% contained GABA immunoreactivity. However, no neurons contained both serotonin and tyrosine hydroxylase staining, and less than 1% displayed both serotonin and GABA immunoreactivities. Cultured serotonergic neurons did not exhibit pacemaker firing in the presence of alpha 1 adrenergic receptor agonists such as phenylephrine or norepinephrine. Approximately one third were hyperpolarized by serotonin or the selective serotonin1A receptor agonist, (+/-)-8-hydroxy-2-(di-N-propylamino)tetralin. Virtually all serotonergic neurons responded to application of glutamate, kainate, N-methyl-D-aspartate, GABA, and glycine. Depolarizing and hyperpolarizing synaptic potentials blocked by glutamate or GABAA receptor antagonists were frequently observed in both serotonergic and non-serotonergic raphe neurons. Slow inhibitory postsynaptic potentials were evoked by activating single presynaptic serotonergic neurons with a brief intracellular current pulse. The slow inhibitory synaptic potential had a mean latency to onset of 35 +/- 5 ms, a duration of 0.8-2.6 s, and was inhibited by the serotonin1A autoreceptor antagonists, (-)propranolol and spiperone. The rising and falling phases of the inhibitory potential could be fit by single exponential functions with mean time constants of 53 +/- 8 ms and 504 +/- 78 ms, respectively. Serotonin1A receptor-mediated autoinhibition was observed in microcultures containing a solitary serotonergic neuron, and thus constituted synaptic serotonin release, responsiveness, and re-uptake by a single vertebrate neuron. In summary, histochemical and electrophysiological evidence was obtained for catecholaminergic, GABAergic, and glutamatergic non-serotonergic raphe neurons in culture, many of which formed functional synaptic connections with neighboring cells. Additionally, cultured mesopontine serotonergic neurons expressed many of the cytochemical markers, neurotransmitter receptors, and synaptic functions observed in such cells in vivo, but the proportion of neurons sensitive to serotonergic and adrenergic agonists was significantly less than that reported in vivo. For the first time, the kinetics and pharmacology of serotonergic synaptic transmission by a single vertebrate serotonergic raphe neuron were determined, and found to resemble those observed after extracellular stimulation of populations of raphe neurons in slices and in vivo.

5,7-Dihydroxytryptamine↗

PubMed1980

Convulsants antagonise inhibition in the olfactory cortex slice.

The effects of some gamma-aminobutyric acid (GABA) antagonists and other "convulsants" have been tested on neurones of the isolated olfactory cortex slice preparation of the guinea-pig using single cell intracellular and gross extracellular recording techniques. Bicuculline, picrotoxin, strychnine, leptazol, bemegride, and also theophylline and d-tubocurarine all increased the duration and amplitude of the excitatory postsynaptic potential, thereby producing a seizure-like discharge. These drugs reduced and shortened the peak conductance increase during the inhibitory postsynaptic potential (i.p.s.p.) in normal solution and after the i.p.s.p. had been prolonged by the presence of a barbiturate. The results suggested that these drugs antagonise synaptic inhibition through a common mechanism, perhaps by reducing the effect of neurally released GABA.

Animals↗

PubMed1964

ELECTROPHYSIOLOGY OF THE FETAL SPINAL CORD. II. INTERACTION AMONG PERIPHERAL INPUTS AND RECURRENT INHIBITION.

Interactions of peripheral inputs to the motoneuron of the kitten fetus as young as 3 weeks prenatal were studied by reflex discharge from the ventral root as well as by recording from single motoneurons. Facilitation was found between two synergists in fetuses 1 to 2 weeks before birth. Intracellular recording showed that the facilitation could be explained by summation of excitatory postsynaptic potentials. Inhibition was found between antagonists in the fetuses 2 to 3 weeks before birth and was accompanied by inhibitory postsynaptic potentials. Recurrent inhibition was very powerful in the fetal spinal cord as shown by large motoneuron hyperpolarization by antidromic stimulation. Cells presumed to be "Renshaw cells" and which responded to both ortho- and antidromic stimulation with repetitive firing were shown in the 2 weeks prenatal fetus. These results lead to the conclusion that there is considerable effective synaptic connection of afferent collaterals already established by the later stage of intrauterine life and that this may be achieved independently of external stimuli.

Axons↗

PubMed1989

Inhibition of inspiratory neurons of the nucleus retroambigualis by expiratory neurons of the Botzinger complex in the cat.

The connection between expiratory neurons of the Botzinger Complex and contralateral inspiratory neurons of the nucleus retroambigualis was examined using the technique of spike-triggered averaging of intracellular potentials. Out of a total of 34 expiratory neurons found in the Botzinger Complex, 25 (73%) could be antidromically activated from the inspiratory region of the contralateral nucleus retroambigualis. The spike activities of 15 of these antidromically activated expiratory neurons were used as triggers for the averaging of the intracellular potentials recorded from 39 inspiratory neurons in the region of the contralateral nucleus retroambigualis. Unitary, inhibitory, postsynaptic potentials were observed in 11 of the 39 (28%) averages, from 6 of the 15 (40%) trigger neurons. It was concluded that these experiments demonstrate a monosynaptic inhibitory connection from expiratory neurons in the Botzinger Complex to inspiratory neurons in the contralateral nucleus retroambigualis.

Action Potentials↗

PubMed1998

Synaptic inputs to stellate cells in the ventral cochlear nucleus.

Auditory information is carried from the cochlear nuclei to the inferior colliculi through six parallel ascending pathways, one of which is through stellate cells of the ventral cochlear nuclei (VCN) through the trapezoid body. To characterize and identify the synaptic influences on T stellate cells, intracellular recordings were made from anatomically identified stellate cells in parasagittal slices of murine cochlear nuclei. Shocks to the auditory nerve consistently evoked five types of synaptic responses in T stellate cells, which reflect sources intrinsic to the cochlear nuclear complex. 1) Monosynaptic excitatory postsynaptic potentials (EPSPs) that were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX), an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, probably reflected activation by auditory nerve fibers. Electrophysiological estimates indicate that about five auditory nerve fibers converge on one T stellate cell. 2) Disynaptic, glycinergic inhibitory postsynaptic potentials (IPSPs) arise through inhibitory interneurons in the VCN or in the dorsal cochlear nucleus (DCN). 3) Slow depolarizations, the source of which has not been identified, that lasted between 0.2 and 1 s and were blocked by -2-amino-5-phosphonovaleric acid (APV), the N-methyl-D-aspartate (NMDA) receptor antagonist. 4) Rapid, late glutamatergic EPSPs are polysynaptic and may arise from other T stellate cells. 5) Trains of late glycinergic IPSPs after single or repetitive shocks match the responses of D stellate cells, showing that D stellate cells are one source of glycinergic inhibition to T stellate cells. The source of late, polysynaptic EPSPs and IPSPs was assessed electrophysiologically and pharmacologically. Late synaptic responses in T stellate cells were enhanced by repetitive stimulation, indicating that the interneurons from which they arose should fire trains of action potentials in responses to trains of shocks. Late EPSPs and late IPSPs were blocked by APV and enhanced by the removal of Mg2+, indicating that the interneurons were driven at least in part through NMDA receptors. Bicuculline, a gamma-aminobutyric acid-A (GABAA) receptor antagonist, enhanced the late PSPs, indicating that GABAergic inhibition suppresses both the glycinergic interneurons responsible for the trains of IPSPs in T-stellate cells and the interneuron responsible for late EPSPs in T stellate cells. The glycinergic interneurons that mediate the series of IPSPs are intrinsic to the ventral cochlear nucleus because long series of IPSPs were recorded from T stellate cells in slices in which the DCN was removed. These experiments indicate that T stellate cells are a potential source of late EPSPs and that D stellate cells are a potential source for trains of late IPSPs.

Action Potentials↗

PubMed1996

Synaptic interactions between primate precentral cortex neurons revealed by spike-triggered averaging of intracellular membrane potentials in vivo.

To document synaptic interactions between neurons in the precentral cortex of macaque monkeys, we recorded in vivo the intracellular (IC) membrane potentials of cortical neurons simultaneously with extracellular (EC) action potentials of neighboring cells. The synaptic potentials correlated with EC spikes were obtained by spike-triggered averages (STA) of the IC membrane potentials for 373 cell pairs recorded in anesthetized and awake behaving monkeys. Sixty-three STAs (17%) showed excitatory postsynaptic potentials (EPSPs), beginning after the trigger spike. Pure EPSPs had onset latencies of 0.9 +/- 0.7 msec (mean +/- SD) and amplitudes of 226 +/- 130 microV. Sixteen STAs (4%) showed postspike inhibitory postsynaptic potentials (IPSPs), with onset latencies of 0.4 +/- 0.4 msec and amplitudes of -274 +/- 188 microV. The most common waveform, observed in 82% of the STAs with features, was a broad depolarization straddling the trigger spikes, reflecting synchronized synaptic input to both IC and EC neurons. These average synchronous excitation potentials (ASEPs) began 14.3 +/- 6.6 msec before the trigger spike and had amplitudes of 1064 +/- 867 microV. Twenty-three STAs (6%) showed an average synchronous inhibitory potential (ASIP): a hyperpolarization beginning before the trigger spike and reflecting IPSPs produced by a group of local inhibitory cells synchronized with the trigger cell. ASIPs had an onset latency of -5.5 +/- 2.7 msec and amplitude of -589 +/- 502 microV. Combinations of synchronous and postspike potentials were also observed. Successive recordings provided examples of convergent and divergent connections between EC and IC cells. Neuron pairs with depolarizing postsynaptic potentials (PSPs) in the STA yielded peaks in the cross-correlograms of the IC and EC action potentials; the peak area was proportional to the amplitude of the PSP. These data suggest that a significantly larger proportion of cortical neurons interact through synchronous activity than through simple serial interactions; moreover, synchronous excitation affected more widely separated cell pairs than EPSPs and IPSPs, which were seen most often among the closest cells.

Action Potentials↗