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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↗

PubMed2005

Entorhinal cortex entrains epileptiform activity in CA1 in pilocarpine-treated rats.

Layer III neurons of the medial entorhinal cortex (mEC) project to CA1 via the temporoammonic pathway and exert a powerful feed-forward inhibition of CA1 pyramidal neurons. The present study evaluates the hypothesis that disrupted inhibition of CA1 pyramidal neurons causes an eased propagation of entorhinal seizures to the hippocampus via the temporoammonic pathway. Using a method to induce a confined epileptic focus in brain slices, we investigated the spread of epileptiform activity from the disinhibited mEC to CA1 in control and pilocarpine-treated rats that had displayed status epilepticus and spontaneous recurrent seizures. In pilocarpine-treated rats, the mEC showed a moderate layer III cell loss and an enhanced susceptibility to epileptiform discharges compared to control animals. Entorhinal discharges propagated to CA1 in pilocarpine-treated rats but not in controls. Disconnecting CA3 from CA1 did not affect the spread of epileptiform activity to CA1 excluding its propagation via the trisynaptic hippocampal loop. Mimicking the invasion of epileptiform discharges by repetitive stimulation of the temporoammonic pathway caused a facilitation of field potentials in CA1 that were contaminated by population spikes and afterdischarges in pilocarpine-treated but not control rats. Single cell recordings of CA1 pyramidal neurons revealed a dramatic loss of feed-forward inhibition and the occurrence of strong postsynaptic excitatory potentials in pilocarpine-treated rats. Excitatory responses in CA1 were characterized by multiple NMDA receptor-mediated afterdischarges and a strong paired-pulse facilitation in response to activation of the temporoammonic pathway. Our results suggest that, irrespective of the enhanced seizure-susceptibility of the mEC in epileptic rats, the loss of feed-forward inhibition and the enhanced NMDA receptor-mediated excitability CA1 pyramidal cells ease the spread of epileptiform activity from the mEC to CA1 via the temporoammonic pathway bypassing the classical trisynaptic hippocampal loop.

Animals↗

PubMed2005

[Effects of milnacipran on neuronal excitability and synaptic transmission in neurons of the rat locus coeruleus].

Effects of milnacipran (MIL), a selective serotonin and noradrenaline (NA) reuptake inhibitor, on the neuronal excitability and synaptic transmission in the rat locus coeruleus (LC) were examined by intracellular and whole-cell patch-clamp recording techniques. We compared MIL and methylphenidate (MPH), a selective NA and dopamine reuptake inhibitor, as a therapeutic agent for attention deficit/hyperactivity disorder. Application of MPH (1-100 microM) and MIL (1-100 microM) to artificial cerebrospinal fluid (ACSF) produced a hyperpolarizing response in LC neurons in a concentration-dependent manner. Spontaneous firing of LC neurons was blocked during the hyperpolarization. The MIL-induced hyperpolarization was blocked by yohimbine (1 microM), an antagonist for alpha-adrenoceptors. These results suggest that the MIL-induced hyperpolarization is mediated by NA via alpha2-adrenoceptors in LC neurons. Under the whole-cell patch-clamp condition, prolonged application of MIL produced an outward current which lasted as long as MIL existed in the ACSF. The outward current induced by NA was enhanced by MIL in LC neurons. MIL enhanced the amplitude and duration of the inhibitory postsynaptic potential, while it depressed the excitatory postsynaptic potential. The results indicated that both MIL and MPH showed almost the same effects on neuronal activity and synaptic transmission in the rat LC. These results suggest that MIL increases the concentration of NA at synaptic clefts by inhibiting the NA reuptake system in the rat LC.

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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)

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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.

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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.

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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)

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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.

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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.

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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↗

PubMed1989

Tongue-muscle-controlling motoneurons in the Japanese toad: neural inputs from the thalamus.

The anuran tongue is an effector organ specialized for snapping up prey during visually guided prey-catching behavior. As a step toward elucidating the control mechanisms of the tongue movement and overall organization of visually guided behavior, properties of neural inputs from the thalamus (of which electrical stimulation elicited a behavior very similar to the visually guided predator-avoidance behavior under freely behaving conditions) were investigated in paralyzed Japanese toads. Tongue-muscle-controlling motoneurons (tongue-protractor motoneurons (PMNs) and tongue-retractor motoneurons (RMNs)) were identified antidromically, and synaptic inputs in response to electrical stimuli applied to various points in the thalamus (mainly the posterocentral thalamic nucleus) were examined. Hyperpolarizing potentials were evoked in both PMNs and RMNs in response to single electrical stimuli applied to the thalamus contralateral or ipsilateral to the recording side. Since these potentials reversed to depolarizing ones after injecting Cl- ions into the cell interior, these hyperpolarizing potentials were concluded to be the usual fast type of inhibitory postsynaptic potentials (IPSPs). On the other hand, depolarizing potentials which were superimposed on the underlying IPSPs were evoked when repetitive electrical stimuli were applied to the thalamus. The amplitude of these depolarizing potentials was decreased when depolarizing currents were injected intracellularly, while it was increased when hyperpolarizing currents were injected, indicating that these depolarizing potentials are excitatory postsynaptic potentials (EPSPs).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1998

Intrinsic primary afferent neurons of the intestine.

After a long period of inconclusive observations, the intrinsic primary afferent neurons of the intestine have been identified. The intestine is thus equipped with two groups of afferent neurons, those with cell bodies in cranial and dorsal root ganglia, and these recently identified afferent neurons with cell bodies in the wall of the intestine. The first, tentative, identification of intrinsic primary afferent neurons was by their morphology, which is type II in the terminology of Dogiel. These are multipolar neurons, with some axons that project to other nerve cells in the intestine and other axons that project to the mucosa. Definitive identification came only recently when action potentials were recorded intracellularly from Dogiel type II neurons in response to chemicals applied to the lumenal surface of the intestine and in response to tension in the muscle. These action potentials persisted after all synaptic transmission was blocked, proving the Dogiel type II neurons to be primary afferent neurons. Less direct evidence indicates that intrinsic primary afferent neurons that respond to mechanical stimulation of the mucosal lining are also Dogiel type II neurons. Electrophysiologically, the Dogiel type II neurons are referred to as AH neurons. They exhibit broad action potentials that are followed by early and late afterhyperpolarizing potentials. The intrinsic primary afferent neurons connect with each other at synapses where they transmit via slow excitatory postsynaptic potentials, that last for tens of seconds. Thus the intrinsic primary afferent neurons form self-reinforcing networks. The slow excitatory postsynaptic potentials counteract the late afterhyperpolarizing potentials, thereby increasing the period during which the cells can fire action potentials at high rates. Intrinsic primary afferent neurons transmit to second order neurons (interneurons and motor neurons) via both slow and fast excitatory postsynaptic potentials. Excitation of the intrinsic primary afferent neurons by lumenal chemicals or mechanical stimulation of the mucosa appears to be indirect, via the release of active compounds from endocrine cells in the epithelium. Stretch-induced activation of the intrinsic primary afferent neurons is at least partly dependent on tension generation in smooth muscle, that is itself sensitive to stretch. The intrinsic primary afferent neurons of the intestine are the only vertebrate primary afferent neurons so far identified with cell bodies in a peripheral organ. They are multipolar and receive synapses on their cell bodies, unlike cranial and spinal primary afferent neurons. They communicate with each other via slow excitatory synaptic potentials in self reinforcing networks and with interneurons and motor neurons via both fast and slow EPSPs.

Animals↗

PubMed1987

Antagonist discrimination of two muscarinic responses elicited by applied agonists and orthodromic stimuli in superior cervical ganglion of rabbit.

Pirenzepine and gallamine selectively and differentially antagonized two muscarinic responses, in the superior cervical ganglion of the rabbit, whether elicited by the muscarinic agonist methacholine or by orthodromic stimulation. Methacholine elicited a biphasic ganglionic response, consisting of hyperpolarizing and depolarizing components that were the agonist-induced equivalents of the slow-inhibitory and slow-excitatory postsynaptic potentials elicited by orthodromic stimulation. Superfusion of ganglia with pirenzepine resulted in a concentration-dependent suppression of depolarization induced by methacholine with no suppressant action on ganglionic hyperpolarization. In contrast, superfusion of ganglia with gallamine resulted in a concentration-dependent suppression of ganglionic hyperpolarization and the slow-inhibitory postsynaptic potential. These effects occurred without appreciable suppression of ganglionic depolarization or the slow-excitatory postsynaptic potential. The action of gallamine was specific for muscarinic hyperpolarization. Hyperpolarizations produced by superfusion with dopamine or norepinephrine were unaffected by gallamine, at concentrations that suppressed the muscarinic slow-inhibitory post-synaptic potential. Incubation with anti-cholinesterases produced a parallel shift, to the right, of concentration-response curves for suppression by gallamine of the slow-inhibitory postsynaptic potential. This was presumably the consequence of an increase in the acetylcholine available for interaction with the muscarinic receptor. The evidence suggests that the ability of gallamine and pirenzepine to suppress selectively the slow-inhibitory and slow-excitatory postsynaptic potentials, as previously demonstrated, is through an action at muscarinic receptors. Furthermore, the data suggest that these pharmacological agents produce their effects by interaction at different muscarinic recognition sites.

Animals↗

PubMed1978

Pentobarbital: differential postsynaptic actions on sympathetic ganglion cells.

The frog sympathetic ganglion has been used as a model to elucidate the cellular mechanism of barbiturate anesthesia. Anesthetic concentrations of pentobarbital markedly reduced the fast nicotinic excitatory postsynaptic potential while having no effect on the slow excitatory postsynaptic potential or slow inhibitory postsynaptic potential, even though all three synaptic potentials depend on the presynaptic release of acetylcholine. A similar differential effect was seen for nicotinic and muscarinic responses to exogenously applied agonists, while the depolarizing action of gamma-aminobutyric acid (GABA) was enhanced. These results indicate that pentobarbital has remarkably selective actions on the sympathetic ganglion and further indicate that blockade of ganglionic transmission by anesthetic concentrations of pentobarbital can be entirely explained by a postsynaptic action. The present results strengthen the concept that pentobarbital anesthesia results from a postsynaptic blockade of central excitatory synapses which increase sodium conductance coupled with a postsynaptic enhancement of GABA-mediated synaptic inhibition.

Animals↗