SEARCH · PubMed Health

Results for “Excitatory 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 307 records · Page 17Linked to original sources

PubMed1979

Avermectin B1a irreversibly blocks postsynaptic potentials at the lobster neuromuscular junction by reducing muscle membrane resistance.

Avermectin B1a, a macrocyclic lactone with broad spectrum anthelmintic activity, affects neuromuscular transmission in the lobster stretcher muscle. Perfusion of the muscle with 1-10 microgram of the drug per ml eliminates inhibitory postsynaptic potentials within a few minutes. Intracellularly recorded excitatory postsynaptic potentials are gradually reduced in amplitude over 20-30 min, and their falling phases become faster; there is no effect, however, on extracellularly recorded excitatory potentials. Avermectin B1a reduced the input resistance of the muscle fibers with a time course similar to that of the reduction of excitatory potentials. Washing for up to 2 hr with drug-free solution fails to reverse the drug's effects. However, perfusion with 20 microgram of picrotoxin per ml results in recovery of the excitatory potentials and input resistance. Avermectin B1a also blocks the firing of the crayfish stretch receptor neuron, and this block is also reversed by picrotoxin. We hypothesize that the reduction in excitatory postsynaptic potentials after avermectin B1a treatment is caused solely by reduction in membrane resistance; additional experiments suggest that the reduction in membrane resistance is due to the opening of membrane Cl- channels, perhaps including those regulated by gamma-aminobutyric acid at the inhibitory synapse.

Animals↗

PubMed2002

Extracellular magnesium ion modifies the actions of volatile anesthetics in area CA1 of rat hippocampus in vitro.

BACKGROUND: Magnesium ion (Mg2+) is involved in important processes as modulation of ion channels, receptors, neurotransmitter release, and cell excitability in the central nervous system. Although extracellular Mg2+ concentration ([Mg2+]o) can be altered during general anesthesia, there has been no evidence for [Mg2+]o-dependent modification of anesthetic actions on neural excitability in central nervous system preparations. The purpose of current study was to determine whether the effects of volatile anesthetics are [Mg2+]o-dependent in mammalian central nervous system. METHODS: Extracellular electrophysiologic recordings from CA1 neurons in rat hippocampal slices were used to investigate the effects of [Mg2+]o and anesthetics on population spike amplitude and excitatory postsynaptic potential slope. RESULTS: The depression of population spike amplitudes and excitatory postsynaptic potential slopes by volatile anesthetics were significantly dependent on [Mg2+]o. The effects were attenuated in the presence of a constant [Mg2+]o/extracellular Ca2+ concentration ratio. However, neither N-methyl-d-aspartate receptor antagonists nor a non-N-methyl-d-aspartate receptor antagonist altered the [Mg2+]o-dependent anesthetic-induced depression of population spikes. Volatile anesthetics produced minimal effects on input-output (excitatory postsynaptic potential-population spike) relations or the threshold for population spike generation. The effects were not modified by changes in [Mg2+]o. In addition, the population spike amplitudes, elicited via antidromic (nonsynaptic) stimulation, were not influenced by [Mg2+]o in the presence of volatile anesthetics. CONCLUSIONS: These results provide support that alteration of [Mg2+]o modifies the actions of volatile anesthetics on synaptic transmission and that the effects could be, at least in part, a result of presynaptic Ca2+ channel-related mechanisms.

2-Amino-5-phosphonovalerate↗

PubMed1987

[Effect of trimebutine on cholinergic transmission in neurons of the inferior mesenteric ganglion of the rabbit].

We analyzed the effects of trimebutine on the synaptic activity of neurons of the rabbit inferior mesenteric ganglion, using intracellular recording techniques. The synaptic activity was produced by subthreshold stimuli (0.5 Hz) applied individually, on lumbar splanchnic and lumbar colonic nerves. These stimuli triggered cholinergic responses corresponding to fast excitatory postsynaptic potentials. In 8 of 20 neurones tested trimebutine (10(-6) g/ml) produced an inhibition of excitatory postsynaptic potentials, without any change in the resting membrane potential. In 6 of 20 neurons tested, trimebutine produced, successively, an early facilitation followed by a late inhibition of excitatory postsynaptic potentials. Both effects occurred without change in the resting membrane potential. The inhibitory and facilitatory effects of trimebutine were accompanied, by an increase and a decrease in the number of failures of nerve stimulation respectively. These results indicate that inhibitory and facilitatory effects of trimebutine correspond respectively to a decrease and an increase in the amount of acetylcholine released from presynaptic nerve terminals originating from the spinal cord and the distal colon.

Acetylcholine↗

PubMed1992

Synaptic mechanisms in sympathetic preganglionic neurons.

Intracellular recordings from sympathetic preganglionic neurons (SPNs) in adult cat and neonatal rat spinal cord slices reveal four types of synaptic potentials, namely, excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and slow EPSPs in both preparations, and a slow IPSP in cat SPNs. Pharmacological studies show that glutamate or a related excitatory amino acid and glycine are the probable mediators of EPSPs and IPSPs. There may be heterogenous mediators of slow EPSPs; substance P, serotonin, norepinephrine, and epinephrine are all probable mediators of slow EPSPs in subpopulations of SPNs. In the case of slow IPSPs, norepinephrine appears to be the likely transmitter. Finally, stimulation of ventral roots elicits a synaptic potential that appears to be caused by glutamate released from afferent fibers in the ventral roots. Our results indicate that a multitude of synaptic mechanisms exist in the rat SPNs by means of which inputs arising from sensory and supraspinal neurons are processed in a timely and orderly manner, thus ensuring highly organized but differentiated outputs to multiple peripheral target cells.

Animals↗

PubMed1990

Mu opioid receptor activation reduces inhibitory postsynaptic potentials in hippocampal CA3 pyramidal cells of rat and guinea pig.

Using intracellular recording techniques, we characterized synaptic responses of CA3 pyramidal cells to mu and kappa agonists in hippocampal slices from rats and guinea pigs. In rat CA3 pyramidal cells, the mu selective agonist (N-MePhe3,D-Pro4)-morphiceptin (PLO17) inhibited both the early and the late inhibitory postsynaptic potentials (IPSPs) and increased excitatory postsynaptic potential (EPSP) amplitudes. Voltage clamp analysis of synaptic currents indicated that the excitatory postsynaptic current were not increased by PLO17, showing that the apparent increase in EPSPs was a result of a decrease in the underlying IPSP. The kappa agonists trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate and dynorphin A (1-17) had no effect on EPSPs or IPSP conductances measured in rat pyramidal cells. Maximal inhibition of IPSPs by PLO17 resulted in a bursting response to stimulation in rat but not guinea pig CA3 pyramidal cells. In guinea pig CA3 pyramidal cells, PLO17 also inhibited IPSP conductances but did not affect EPSP amplitudes. In contrast to the lack of effect in rat pyramidal cells, trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate (100 nM) inhibited the late IPSP conductance without influencing the EPSP or the early IPSP conductance of guinea pig pyramidal cells. Dynorphin A (1-17) (0.01-10 microM) did not affect resting membrane properties or evoked synaptic conductances in either preparation. Mu receptor activationin the CA3 of rats and guinea pigs results in the inhibition of inhibitory synaptic input to pyramidal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

In vivo electrophysiological investigations into the role of histamine in the dentate gyrus of the rat.

Drugs acting at the three known classes of histamine receptors were injected intracerebroventricularly into the rat. The effects of these drugs upon synaptic potentials recorded from the dentate gyrus of the freely-moving rat were determined. Population spikes and field excitatory postsynaptic potentials were recorded from the granule cell layer of the dentate gyrus following stimulation of the perforant path. Drugs, dissolved in 0.9% NaCl were applied into the lateral cerebral ventricle in a volume of 5 microl over a period of 6 min. The histamine H1 receptor antagonist mepyramine (0.4 or 0.8 microg) had no significant effect on population spikes or field excitatory postsynaptic potentials. In contrast the H2 receptor antagonist cimetidine (3.25, 6.5 or 13 microg) showed a biphasic effect. At the lower doses (3.25 or 6.5 microg) a small (15%) depression of the field excitatory postsynaptic potentials and population spikes was observed beginning about 1 h following the infusion. At the highest dose tested (13 microg) a marked increase of the population spike was observed beginning immediately following the infusion and lasting for 90 min. Application of the H3 receptor agonist R-alpha-methylhistamine (0.2 microg) depressed the field excitatory postsynaptic potentials (15% at 4 h post-injection) and even more strongly the population spike (50%). Surprisingly, at higher doses (0.4 and 0.8 microg) no effect was seen. The H3 receptor antagonist thioperamide (0.41 and 0.82 microg) did not cause an increase in synaptic potentials but rather at the highest dose a small depression occurred at later time points (2-4 h following the infusion). At the lower dose (0.41 microg) thioperamide blocked the effect of R-alpha-methylhistamine (0.2 microg). These results show that the histaminergic system modulates information flow through the dentate gyrus in a complex manner involving both histamine H2 and H1 receptors.

Animals↗

PubMed2000

Characterization of synaptic transmission in the ventrolateral periaqueductal gray of rat brain slices.

Synaptic transmission evoked by focal stimulation in the ventrolateral periaqueductal gray was characterized using the whole-cell recording technique in rat brain slices. At resting membrane potential (-62+/-1 mV), focal stimulation (0.05-0.1 ms, 0.03 Hz) usually evoked a 6-cyano-7-nitroquinoxaline-2, 3-dione-sensitive fast excitatory postsynaptic potential and a DL-2-amino-5-phosphonopentanoic acid-sensitive slow excitatory postsynaptic potential with a bicuculline-sensitive inhibitory postsynaptic potential in between. In the presence of kynurenic acid, bicuculline-sensitive inhibitory postsynaptic currents recorded in the voltage-clamp mode displayed a reversal potential of -68+/-3 mV, resembling GABA(A) receptor-mediated inhibitory postsynaptic currents. However, no GABA(B) receptor-mediated inhibitory postsynaptic current was evoked, even at stronger stimulating intensity. 6-Cyano-7-nitroquinoxaline-2,3-dione-sensitive fast excitatory postsynaptic currents were isolated by DL-2-amino-5-phosphonopentanoic acid plus bicuculline and DL-2-amino-5-phosphonopentanoic acid-sensitive slow fast excitatory postsynaptic currents by bicuculline plus 6-cyano-7-nitroquinoxaline-2,3-dione. Both types of excitatory postsynaptic current reversed at potentials near 0 mV. The I-V curve of slow fast excitatory postsynaptic currents or N-methyl-D-aspartate currents displayed a negative slope at potentials more negative than -30 mV in an Mg(2+)-sensitive manner. The control postsynaptic currents reversed at potentials between -50 and -35 mV, inclined to the reversal potential of GABA(A), but not glutamate, receptor channels. It is concluded that, in the ventrolateral periaqueductal gray, focal stimulation elicits both inhibitory and excitatory transmission, while the former is dominant. The inhibitory transmission is mediated by GABA(A) but not GABA(B) receptors. The excitatory transmission is mediated by glutamate acting on alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate as well as N-methyl-D-aspartate receptors.

Animals↗

PubMed1971

Synaptic transmission in the crayfish: increased release of transmitter substance by bacterial endotoxin.

Bacterial endotoxin increases the frequency of miniature excitatory postsynaptic potentials, decreases facilitation, and increases the evoked excitatory postsynaptic potential without changing membrane resistance. These data indicate that endotoxin acts on the presynaptic nerve terminal by increasing the amount of transmitter substance released in response to an applied stimulus.

Animals↗

PubMed1994

Cerebellar-responsive neurons in the thalamic ventroanterior-ventrolateral complex of rats: in vivo electrophysiology.

In vivo intracellular recordings were obtained from identified thalamocortical neurons in the ventroanterior-ventrolateral complex in urethane-anesthetized rats. This thalamic nucleus has few interneurons. Neurons that responded to cerebellar stimulation were injected intracellularly with horseradish peroxidase or biocytin and examined with light and electron microscopy (see companion paper). Intrinsic membrane properties and voltage-dependent rhythmic activity of cerebellar-responsive ventroanterior-ventrolateral neurons were similar to those described previously for thalamic neurons. Thus, in addition to conventional "fast" Na(+)-dependent spikes, rat ventroanterior-ventrolateral neurons had "slow" Ca(2+)-mediated low-threshold spikes and membrane conductances that supported rhythmic oscillations. Two modes of spontaneous activity were observed: (i) a tonic firing pattern that consisted of irregularly occurring fast spikes that predominated when the membrane potential was more positive than about -60 mV, and (ii) a rhythmic firing pattern, observed when the membrane potential was more negative than about -65 mV, composed of periodic (4-8 Hz) membrane hyperpolarizations and ramp depolarizations that often produced a low-threshold spike and a burst of fast spikes. In some neurons, spontaneous fast prepotentials were also observed, often with a relatively constant rate (up to 70 Hz). Cerebellar stimulation elicited excitatory postsynaptic potentials that in some cases appeared to be all-or-none and were similar in form to fast prepotentials. Stimulation of ipsilateral motor cortex elicited a short-latency antidromic response followed by a monosynaptic excitatory postsynaptic potential, which had a slower rise time than excitatory postsynaptic potentials evoked from cerebellum, suggesting that cortical inputs were electrotonically distal to cerebellar inputs. In the presence of moderate membrane hyperpolarization, the cortically evoked excitatory postsynaptic potential was followed by a long-lasting hyperpolarization (100-400 ms duration), a rebound depolarization and one or two cycles resembling spontaneous rhythmic activity. Membrane conductance was increased during the initial component of the long hyperpolarization, much of which was probably due to an inhibitory postsynaptic potential. In contrast, membrane conductance was unchanged or slightly decreased during the latter three-quarters of the long hyperpolarization. The amplitude of this component of the long hyperpolarization usually decreased when the membrane was hyperpolarized with intracellular current injection. Thus, both disfacilitation and an inhibitory postsynaptic potential may have contributed to the latter portion of the cortically-evoked long hyperpolarization. The cortically-evoked inhibitory postsynaptic potentials likely originated predominantly from feedforward activation of GABAergic neurons in the thalamic reticular nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1990

[A quantal analysis of the long-term potentiation of the total postsynaptic neuronal potentials in surviving hippocampal slices].

Excitatory postsynaptic potentials (EPSPs) from 14 neurons have been recorded in hippocampal slices (area CA1) of guinea pigs after stimulation of stratum radiatum (Schaffer collaterals) and stratum oriens. An increase of EPSP amplitudes observed in 7 neurons (9 pathways) recorded 15-45 min after titanic stimulation of Schaffer collaterals is considered as a long-term potentiation (LTP). A statistical analysis in the frame of two methods of the quantal hypothesis (histogram and variance methods) has shown an increase in the mean quantal content (m) during LTP. An increase in the quantal size found only by the histogram method is considered to be less reliable because comparatively strong dependence of the histogram method on the noise level. An increase in m revealed by two methods corresponds to the previous in vivo studies and favours a presynaptic location of mechanisms responsible for the growth of the synaptic efficacy during LTP.

Animals↗

PubMed1991

Frequency potentiation in granule cells in vivo at theta frequency perforant path stimulation.

The effect of frequency potentiation on the postsynaptic potential in granule cells was studied stimulating the perforant path in curarized and urethanized rats. At stimulation frequencies between 2.0-5.0 Hz, synaptic efficacy in eliciting an orthodromic action potential increased despite the hyperpolarization of the transmembrane potential. The excitatory postsynaptic potential (EPSP) slope and duration also increased while the inhibitory postsynaptic potential (IPSP) was reduced. Stimulation frequencies greater than 5.0 Hz produced similar changes in the transmembrane potential and EPSP-IPSP sequence, but they did not increase synaptic efficacy. The frequency potentiation at frequencies into the theta band suggest that this potentiation participates in theta rhythm genesis in this structure which, in turn, suggests that the fascia dentata could work as a band-pass filter. In 12.5% of cases postpotentiation was also observed.

Action Potentials↗

PubMed1995

Nitric oxide is used as an orthograde cotransmitter at identified histaminergic synapses.

1. Nitric oxide (NO) is produced by the enzyme nitric oxide synthase (NOS) and serves as an interneuronal messenger. Here, an identified histaminergic neuron (C2) in the mollusk Aplysia californica is shown to contain NOS with the use of NADPH diaphorase staining, suggesting that NO and histamine are used as cotransmitters by neuron C2. 2. The NOS containing neuron, C2, evokes a very slow excitatory postsynaptic potential in two of its identified postsynaptic follower neurons that are insensitive to H1 and H2 histamine receptor antagonists. 3. The very slow excitatory postsynaptic potential is blocked by inhibitors of NOS, such as nitroarginine methyl ester, and suppressed by the NO scavenger reduced hemoglobin. 4. Treatments with compounds that release NO, such as nitrosocysteine, mimic the membrane depolarization and the decrease in membrane conductance in the follower that are characteristic of the very slow excitatory postsynaptic potential induced normally by the presynaptic C2 neuron. 5. These results indicate that NO is used as an orthograde synaptic cotransmitter at synapses between histaminergic neuron C2 and its followers that receive the very slow excitatory postsynaptic potential.

Animals↗

PubMed1993

Long-lasting potentiation of synaptic transmission in the Schaffer collateral-commissural pathway of the guinea pig hippocampus by activation of postsynaptic N-methyl-D-aspartate receptor.

The effects of short-period (2 min) perfusion of conditioning solution, which contains N-methyl-D-aspartate (NMDA), glycine, and spermine, on the synaptic transmission in the Schaffer collateral-commissural pathway were examined in hippocampal slices with the intracellular recording technique. Long-lasting potentiation of excitatory postsynaptic potentials (EPSPs) was induced (as long as the records lasted, up to 3 h in the longest observation) after membrane potentials of postsynaptic neurons were depolarized by current injection during perfusion of the conditioning solution. D-2-amino-5-phosphonovaleric acid (D-AP5), a specific antagonist of NMDA receptors, block the induction of the long-lasting potentiation by perfusion of NMDA containing solution. This potentiation was accompanied by a decrease in the relative magnitude of EPSP amplitude fluctuation (coefficient of variation, CV). The reciprocals of squared CVs (= mean2/variance) were almost proportional to the magnitude of the potentiation, and the ratios of 1/CV2 and the magnitudes of potentiation were not different from those of long-term potentiation (LTP) induced by tetanic stimulation. These findings suggest that long-lasting potentiation is induced solely by activation of postsynaptic NMDA receptors, and transmitter release from presynaptic terminals may be modified by the activation of postsynaptic receptors.

2-Amino-5-phosphonovalerate↗

PubMed1997

Evidence for involvement of the neuronal isoform of nitric oxide synthase during induction of long-term potentiation and long-term depression in the rat dentate gyrus in vitro.

The possible role of nitric oxide in the induction of long-term potentiation and long-term depression of field excitatory postsynaptic potentials in the dentate gyrus of the hippocampal slice has been investigated, in the rat, using two novel nitric oxide synthase inhibitors, 1-(2-trifluoromethylphenyl)imidazole, which is selective for the neuronal isoform in vitro, and 3-bromo-7-nitro-indazole. Long-term potentiation was induced by a series of high-frequency trains, and long-term depression was induced by prolonged low-frequency stimulation at 1 Hz. The induction of long-term potentiation was inhibited by both 1-(2-trifluoromethylphenyl)imidazole and 3-bromo-7-nitro-indazole at concentrations which did not alter the amplitude of the test excitatory postsynaptic potential. The inhibitory effect of 1-(2-trifluoromethylphenyl)imidazole on the induction of long-term potentiation was prevented by pretreatment with L-arginine, the substrate amino acid used by nitric oxide synthase for nitric oxide production. The induction of long-term depression was inhibited by both 3-bromo-7-nitro-indazole and 1-(2-trifluoromethylphenyl)imidazole at concentrations which did not affect the test excitatory postsynaptic potential. The inhibitory effect of 1-(2-trifluoromethylphenyl)imidazole was prevented by pretreatment with L-arginine. The present experiments provide strong support for the involvement of the neuronal isoform of nitric oxide synthase in the induction of long-term potentation and long-term depression.

Animals↗

PubMed1995

Methylmercury acts at multiple sites to block hippocampal synaptic transmission.

To explore the mechanisms by which methylmercury (MeHg) blocks central synaptic transmission, intracellular recordings of action potentials and resting membrane potentials were made in CA1 neurons of rat hippocampal slices. At 4 to 100 microM, MeHg blocked action potentials in a concentration- and time-dependent manner. MeHg also depolarized Ca1 neuronal membranes. However, this effect occurred more slowly than block of action potentials because the resting membrane potentials remained unchanged when threshold stimulation-evoked action potentials were blocked. Thus, MeHg may initially alter the threshold level of neuronal membrane excitability and subsequently depolarize the membrane leading to block of synaptic transmission. To identify potential sites of action of MeHg, effects of MeHg on the responses of CA1 neurons to orthodromic stimulation of Schaffer collaterals, antidromic stimulation of the alveus, direct injection of current at cell soma and iontophoretic application of glutamate were compared. At 20 and 100 microM, MeHg blocked action potentials evoked by stimulation of Schaffer collaterals and by current injection at the cell soma at similar times. In contrast, action potentials evoked by stimulation of the alveus were blocked more rapidly by 100 microM MeHg than were action potentials evoked by current injection at CA1 neuronal soma. MeHg also blocked the responses of CA1 neurons to iontophoresis of glutamate, but time to block of these responses was slower than block of the corresponding orthodromically-evoked responses by stimulation of Schaffer collaterals. Compared to excitatory postsynaptic potentials, inhibitory postsynaptic potentials appeared to be more sensitive to MeHg, because block of inhibitory postsynaptic potentials occurred before block of excitatory postsynaptic potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

Glutamate mediates an excitatory influence of the paraventricular hypothalamic nucleus on the dorsal motor nucleus of the vagus.

Data have shown that the paraventricular nucleus of the hypothalamus (PVN) and the dorsal motor nucleus of the vagus (DMNV) play important roles in the regulation of gastrointestinal function and eating behavior. Anatomical studies have demonstrated direct projections from the PVN to the DMNV and physiological studies showed that the DMNV mediates many of the effects of PVN stimulation and electrical current stimulation of the PVN excites a subset of DMNV neurons. The aim of this study was to characterize the role of glutamate receptors in the excitatory influence of the PVN on gut-related DMNV neurons. Using single-cell recording techniques, we determined the effects of kynurenic acid, 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX), and DL-2-amino-5-phosphonopentanoic acid (DL-AP5) on the increase in firing rate due to electrical current stimulation of the PVN. In initial experiments, we studied 24 DMNV neurons excited by electrical current stimulation of the PVN. Kynurenic acid, a broad-spectrum glutamate receptor antagonist, prevented the PVN effect in 22 neurons and significantly attenuated the effect in the other cells. Nine of these neurons demonstrated an inhibition in firing rate with PVN stimulation after pretreatment with kynurenic acid. In a separate group of 12 neurons, we determined the effects of CNQX (1.2 nmol) injected into the DMNV. This AMPA receptor antagonist completely blocked the excitatory response to PVN stimulation of six DMNV neurons and significantly attenuated the response of the other six DMNV neurons. The addition of 1.2 nmol DL-AP5, a N-methyl-D-aspartate (NMDA) receptor antagonist, further attenuated the response to PVN stimulation in four of the five DMNV neurons that were still excited after CNQX treatment. The fifth neuron demonstrated PVN- induced inhibition of firing rate after treatment with CNQX and DL-AP5. In a separate group of 11 DMNV neurons excited by electrical stimulation of the PVN, DL-AP5 partially attenuated the excitatory responses of only four DMNV neurons and did not block the excitation of any cells. The mean latency (14 neurons tested) from the PVN to the DMNV was 37.71 +/- 2.40 (SE) ms. Monosynaptic action potentials and excitatory postsynaptic potentials were demonstrated in three DMNV neurons by intracellular recording. Our results indicate that glutamate released from PVN neurons projecting to the DMNV excite the gut-related vagal motor neurons by acting predominantly on the AMPA receptor. The NMDA receptor plays only a minor role in the excitatory effect.

Animals↗

PubMed1998

Plasticity in an electrosensory system. III. Contrasting properties of spatially segregated dendritic inputs.

Efferent neurons of the first-order electrosensory processing center of the brain, the electrosensory lateral line lobe (ELL), receive electroreceptor afferent input as well as feedback inputs descending from higher centers. These ELL efferents, pyramidal cells, adaptively filter predictable patterns of sensory input while preserving sensitivity to novel stimuli. The filter mechanism involves integration of centrally generated predictive inputs with the afferent inputs being canceled. The predictive inputs, referred to as "negative image" inputs, terminate on pyramidal cell apical dendrites and generate responses that are opposite those resulting from the predictable afference, hence integration of these signals results in attenuation of pyramidal cell responses. The system also shows a robust form of plasticity; the pyramidal cells learn, with a time course of a few minutes, to cancel new patterns of repetitive inputs. This is accomplished by adjusting the strength of excitatory and inhibitory apical dendritic inputs according to an anti-Hebbian learning rule. This study focuses on the properties of two separate pathways that convey descending information to pyramidal cell apical dendrites. One pathway terminates proximally, nearer to the pyramidal cell body, whereas the other terminates distally. Recordings of ELL evoked potentials, extracellular pyramidal cell spike responses, and intracellularly recorded synaptic potentials show that the pyramidal cells respond oppositely to moderate-frequency (> approximately 8 Hz) single pulse stimulation or repeated (1/s) tetanic activation of these two pathways. Repetitive activation of the proximally terminating pathway results in highly facilitating responses due to potentiation of pyramidal cell excitatory postsynaptic potentials (EPSPs). These same stimuli applied to the distally terminating pathway result in a reduction of pyramidal cell responses due to depression of EPSPs and potentiation of inhibitatory postsynaptic potentials (IPSPs). Anti-Hebbian plasticity was demonstrated by pairing tetanic stimulation of either pathway with changes in the postsynaptic cell's membrane potential. After stabilization of the response potentiation due to tetanic stimulation of the proximally terminating pathway, paired postsynaptic hyperpolarization resulted in further increases in spike responses and additional potentiation of pyramidal cell EPSPs. Paired postsynaptic depolarization reduced subsequent responses to the tetanus, depressed EPSP amplitudes, and, in many cases, potentiated IPSPs. The same pattern of plasticity was observed when postsynaptic hyper- or depolarization was paired with tetanic stimulation of the distally terminating pathway except that the plasticity was superimposed on the depressed pyramidal cell responses resulting from stimulating this pathway alone. Modulation of a postsynaptic form of synaptic depression is proposed to account for the anti-Hebbian plasticity associated with both pathways.

Animals↗

PubMed1998

Correlation of electrophysiological and morphological characteristics of myenteric neurons of the duodenum in the guinea-pig.

Intracellular recording, dye filling and immunohistochemistry were used to investigate neurons of the proximal duodenum of the guinea-pig. Recordings were made from neurons of the myenteric plexus in the presence of nicardipine to quell muscle contractions, using microelectrodes that contained the marker substance Neurobiotin. Preparations were subsequently processed histochemically to reveal nerve cell shapes and immunoreactivity for calbindin, calretinin or nitric oxide synthase. Neurons were distinguished by their shapes and axonal projections as Dogiel type II, Dogiel type I, filamentous descending interneurons and small filamentous neurons. Dogiel type II cells had large cell bodies and multiple axon processes. They each had a broad action potential (mean half-width, 2.9 ms) and a prominent inflection (hump) on the falling phase of the action potential. The majority (70%) of Dogiel type II cells were AH neurons, defined by their having a prolonged hyperpolarizing potential that followed a soma action potential and lasted more than 2 s. Fast excitatory postsynaptic potentials were not recorded from Dogiel type II neurons. Two thirds of Dogiel type II neurons fired phasically in response to intracellularly injected 500 ms depolarizing current pulses and one-third fired tonically. Calbindin immunoreactivity occurred in 70% of Dogiel type II neurons. Dogiel type I neurons had lamellar dendrites and a single axon. They had brief action potentials (mean half-width, 1.7 ms) with no, or a slight hump. They responded to fibre tract stimulation with fast excitatory postsynaptic potentials. Only 2/21 exhibited a prolonged hyperpolarization following action potentials. The majority of Dogiel type I neurons thus belong to the S neuron category. Nine Dogiel type I neurons fired phasically in response to 500 ms depolarizing current pulses, while 12 fired tonically. Filamentous descending interneurons had long, branching filamentous dendrites and a single anally-projecting axon which gave rise to varicose branches in myenteric ganglia. Action potential characteristics of filamentous interneurons ranged between those of Dogiel type II and type I neurons. Small neurons. Small neurons with short filamentous, or few simple dendrites were also characterized. They had single axons, which could be traced either locally to the circular muscle, or to the longitudinal muscle. None of 12 filamentous interneurons or of 10 small filamentous neurons exhibited a prolonged post-spike hyperpolarization, whereas fast excitatory postsynaptic potentials were recorded from a majority. It is concluded that the morphological types of neuron that are encountered in the ileum also occur in the duodenum, but the electrophysiological characteristics of the neurons are more variable for each morphological class. Thus, it is not always possible to predict the morphology of myenteric neurons in the duodenum from their electrophysiological properties. Part of the electrophysiological variability appears to be due to duodenal neurons being more excitable than ileal neurons.

Action Potentials↗