Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Synaptic Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 1,693 records · Page 94Linked to original sources
PubMed1983

The synaptic current evoked in cat spinal motoneurones by impulses in single group 1a axons.

Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in motoneurones of anaesthetized cats by impulses in single group 1 a axons. E.p.s.p.s with a time course which indicated a somatic site of origin were voltage-clamped using a single micro-electrode clamp. Excitatory post-synaptic currents (e.p.s.c.s) were found to peak in less than 0.2 ms, and to decay with an exponential time course. The time constant of decay was usually in the range 0.3-0.4 ms (at 37 degrees C). At the resting membrane potential, an e.p.s.p. with a peak of 100 microV was generated by an average peak e.p.s.c. of 330 pA. This corresponded to an average peak conductance increase of 5 nS. The e.p.s.c. decreased with membrane depolarization, and reversed to become an outward current at a null potential of +4.6 +/- 2 mV (+/- S.E. of mean; n = 7). Membrane hyperpolarization caused the peak e.p.s.c. to increase and the time constant of decay of the e.p.s.c. to decrease. The total charge in the synaptic current did not increase with hyperpolarization. This observation can explain earlier observations which showed that the peak amplitude of the e.p.s.p. did not increase with hyperpolarization. The number of ion channels opened by transmitter release at a single somatic bouton was estimated to be in the range 40-240.

Animals↗
PubMed1988

Properties of synaptic transmission at the neuromuscular junction of the squid, Loligo opalescens.

1. Spontaneous and evoked synaptic activity were recorded from the muscles of squid fin and mantle. These spontaneous synaptic potentials were large (up to 30 mV) and pleomorphic. Their amplitudes were not normally distributed, nor did they appear to be clustered in integral multiples of some "unit" event size. 2. Electrical stimulation of the nerve resulted in muscle twitches when the bath calcium concentration was a third normal or higher. The frequency of spontaneous synaptic events was unaffected by low calcium. 3. The large size of spontaneous events may mean that the synchronized release of only a few such "quanta" are sufficient to cause muscle action potentials and contraction. 4. The shapes of spontaneous events correlated poorly with their amplitudes, which is consistent with release from multiple synaptic sites with distinct properties.

Animals↗
PubMed1984

Synaptic mechanisms involved in the inspiratory modulation of vagal cardio-inhibitory neurones in the cat.

The respiratory modulation of the activity of vagal cardio-inhibitory neurones of the nucleus ambiguus of the cat has been investigated by electrophysiological and neuropharmacological techniques. All twenty-four vagal efferent neurones studied had axons with conduction velocities indicative of B fibres and projected to the right cardiac branches of the vagus. Their spontaneous or DL-homocysteic acid (DLH)-evoked activity showed a marked reduction during the phase of inspiration and all showed signs of receiving a baroreceptor input. Ionophoretic application of DLH always excited cardiac vagal motoneurones (c.v.m.s). Application of acetylcholine to these same cells provoked a decrease in firing rate in twelve of the fifteen neurones tested. In ten of these twelve cells simultaneous application of atropine antagonized the effect of acetylcholine. Atropine applied alone enhanced neuronal firing, particularly in inspiration. Stable intracellular recordings have been made from two c.v.m.s. These were inhibited during inspiration. Input resistance fell markedly during inspiration and injection of chloride reversed this wave of hyperpolarization to a wave of depolarization indicating that this resulted from chloride-mediated inhibitory post-synaptic potentials (i.p.s.p.s). These c.v.m.s were activated during Stage I expiration, and showed a weak and variable wave of inhibition in Stage II expiration. Pulse-rhythmic depolarizing potentials were reduced in their amplitudes during the periods of decreased neurone input resistance. It is concluded that c.v.m.s receive an excitatory input during post-inspiration and a powerful inhibitory synaptic input during inspiration. The implications of these observations for the physiology of cardiorespiratory reflexes are discussed.

Acetylcholine↗
PubMed2005

Synaptic transmission mediated by ionotropic glutamate, glycine and GABA receptors in the rat's ventral nucleus of the lateral lemniscus.

The synaptic pharmacology of the ventral nucleus of the lateral lemniscus (VNLL) was investigated in brain slices obtained from rats of 14-37 days old using intracellular recording techniques. Excitatory and inhibitory synaptic potentials (EPSPs and IPSPs) were elicited by electrical stimulation of the lemniscal pathway and recorded from neurons with five types of intrinsic firing patterns (onset, pause, adapting, regular and bursting types). Synaptic receptors that mediated the EPSPs and IPSPs were identified using AMPA, NMDA, GABA(A) and glycine receptor antagonists. The early/short EPSPs were mediated by AMPA receptors. The late/long EPSPs, encountered only in neurons of younger animals, were mediated by NMDA receptors. The IPSPs in most neurons were mediated by glycine receptors. In some neurons the IPSPs were mediated by GABA(A) receptors or both glycine and GABA(A) receptors. The temporal dynamics of fast AMPA EPSPs and glycinergic IPSPs were very similar. AMPA EPSPs and glycinergic (and/or GABAergic) IPSPs could be encountered in a single neuron. The results suggest that the VNLL not only relays incoming signals rapidly from the lower brainstem to the inferior colliculus, but also integrates excitatory and inhibitory inputs to modify and process auditory information.

Animals↗
PubMed1996

Threshold serotonin concentration required to produce synaptic facilitation differs for depressed and nondepressed synapses in Aplysia sensory neurons.

1. The modulatory actions produced by the neurotransmitter serotonin (5HT) in Aplysia sensory neurons (SNs) can be distinguished on the basis of their concentration requirement for 5HT, their activation and recovery kinetics, and their dependence on the relative contribution of different second messenger pathways. In addition, some of the facilitatory mechanisms activated by 5HT appear to be different depending upon the recent activation history of synaptic transmission from the SNs. In this study, we examined the concentration requirements of 5HT-induced facilitation of depressed and nondepressed synapses. 2. In isolated pleural-pedal ganglia, we produced facilitation of monosynaptic connections between tail SNs and motor neurons (MNs), using different concentrations of 5HT. As a measure of each preparation's greatest sensitivity to 5HT, we first determined the lowest 5HT concentration that produced increased excitability in the SNs ("threshold" 5HT). Then, in one series of experiments, we applied 5HT sequentially to the same synapse, first in the nondepressed and then in the depressed state. In a second series, we applied 5HT simultaneously to two SNs connecting to the same MN; one synapse was depressed, the other nondepressed. 3. In both series of experiments, we found that the 5HT concentration required to produce facilitation of depressed excitatory post-synaptic potentials (EPSPs) was invariably lower than the 5HT concentration that produced facilitation of nondepressed EPSPs. In the first series, 'threshold' 5HT (1.6 microM) was sufficient to facilitate the synapse in the depressed state, but not the nondepressed state. However, the nondepressed synapse could still be facilitated by higher concentrations of 5HT (10 microM). In the second series, increased excitability of SNs, facilitation of depressed synapses, and facilitation of nondepressed synapses were progressively recruited as a function of increasing 5HT concentration (4.1, 6.7, and 10-15 microM, respectively). 4. These data are consistent with previous studies suggesting that different cellular mechanisms contribute to the facilitation of depressed and nondepressed synapses. In addition, our results provide a way to experimentally separate the two processes and to analyze them simultaneously and independently. Taking advantage of this dissociation, in future experiments it may be possible to directly compare the relative contributions of different intracellular mechanisms to synaptic facilitation and to relate them to the degree of recent synaptic activation.

Action Potentials↗
PubMed1995

Postnatal development of pre- and postsynaptic GABAB-mediated inhibitions in the CA3 hippocampal region of the rat.

1. Intracellular recordings were made from adult and neonatal rat hippocampal slices to study the postnatal development of GABAB-mediated inhibition in CA3 pyramidal neurons. 2. In the presence of glutamatergic receptor antagonists, direct electrical stimulation of the interneurons induced a biphasic GABAA- and GABAB-mediated inhibitory postsynaptic potential in adult [postnatal day (P) 30-P40] and young (P6-P8) CA3 pyramidal neurons. In contrast, in pups (P0-P3), electrical stimulation only induced a bicuculline-sensitive depolarizing GABAA synaptic potential. 3. The outward postsynaptic currents generated by bath-applications of baclofen (30 microM, 30 s) at P3 (78 +/- 60 pA, mean +/- SE) were 4 to 5 times smaller than those evoked between P6 (329 +/- 32 pA) and P30 (412 +/- 44 pA). At P0, baclofen failed to induce a postsynaptic current. 4. The outward currents generated by serotonin (50 microM, 30 s) and the A1 receptor agonist N-cyclopentyladenosine (40 microM, 30 s) ranged between 0 and 50 pA at P3 and between 200 and 400 pA at P6 and P30 (holding potential = -60 +/- 2 mV). 5. In the presence of potassium channel blockers, the amplitude of calcium current elicited by a depolarizing voltage step command (1 s) from a holding potential of -60 mV to a test potential of 0 mV was 2 +/- 0.15 nA at P6 (n = 9) and 0.73 +/- 0.14 nA at P3 (n = 8). Baclofen reversibly reduced the amplitude of calcium currents in young rats but not in pups. 6. Baclofen reversibly reduced the amplitude of the evoked GABAA-mediated and glutamatergic synaptic events at all developmental stages. These effects were dose dependent and antagonized by P-alpha 3-aminopropyl-P-diethoxymethyl-phosphinic acid (CGP) 35348 (500 microM). 7. We conclude that postsynaptic GABAB-mediated inhibition is absent or minimal during the first postnatal days in the CA3 region. In contrast, presynaptic GABAB inhibition is present at birth. We discuss the mechanisms and physiological consequences of these observations.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

Potentiation of spontaneous synaptic activity in rat mossy cells.

Recent studies have demonstrated the vulnerability of dentate mossy cells to seizure-induced damage. One source of potentially damaging synaptic input are spontaneously active granule cell terminals ('mossy terminals'.) We sought to test whether there were activity-dependent changes in the spontaneous excitatory input to mossy cells. Using the in vitro slice preparation, we examined the frequency and amplitude of spontaneous excitatory postsynaptic potentials (EPSPs) after intracellular current injection designed to mimic the extreme depolarization these neurons receive during repetitive afferent stimulation. In 4 of 7 neurons, depolarization with trains of current pulses resulted in a significant and persistent increase in frequency of spontaneous synaptic depolarizations (to an average of 178% of the initial baseline rate). In 3 of these affected neurons, an increased frequency of large amplitude, fast-rising EPSPs accounted for the majority of this change. Injection of hyperpolarizing current pulses failed to alter spontaneous activity in 3 other mossy cells. These results suggest spontaneous synaptic input to mossy cells in plastic and can be potentiated by depolarization of a single postsynaptic mossy cell. The ability of mossy cells to potentiate their excitatory input may be relevant to their vulnerability to excitotoxic injury during repetitive afferent stimulation.

Animals↗
PubMed1985

Membrane potential and input resistance in alpha motoneurons of hindlimb extensors during isolated and clustered episodes of phasic events in REM sleep.

The function of motoneurons during the phasic events of REM sleep was investigated in cats. The membrane potential, synaptic activity, input resistance and rheobase were measured in hindlimb extensor motoneurons during periods of concentrated phasic events (Type II) in REM sleep in undrugged, minimally restrained cats. During Type II episodes in REM sleep, motoneurons depolarized 3 mV on the average, reduced in input resistance by 20%, and had distinct increases in spontaneous synaptic activity, as compared with periods of REM sleep between episodes (i.e. Type I). This constellation of properties is explained by increased frequencies of both unitary EPSPs and IPSPs in motoneurons. Myoclonic jerks in Type II episodes do not appear to arise because of a temporary withdrawal of the tonic motoneuron inhibition found in REM sleep. Instead, large increases in excitatory synaptic activity overcome the inhibition, giving rise to motoneuron discharges.

Animals↗
PubMed2003

A population of pedal-buccal projection neurons associated with appetitive components of Aplysia feeding behavior.

Backfills of the cerebral-buccal connective (CBC) of Aplysia californica revealed a cluster of five to seven pedal-buccal projection neurons in the anterolateral quadrant of the ventral surface of each pedal ganglion. Intra- and extracellular recordings showed that the pedal-buccal projection neurons shared common electrophysiological properties and synaptic inputs. However, they exhibited considerable heterogeneity with respect to their projection patterns. All pedal-buccal projection neurons that were tested received a slow excitatory postsynaptic potential from the ipsi- and contralateral cerebral-pedal regulator (C-PR) neuron, a cell that is thought to play a key role in the generation of a food-induced arousal state. Tests were conducted to identify potential synaptic follower neurons of the pedal-buccal projection neurons in the cerebral and buccal ganglia, but none were detected. Finally, nerve recordings revealed projections from the pedal-buccal projection neurons in the nerves associated with the buccal ganglion. In tests designed to determine the functional properties of these peripheral projections, no evidence was obtained supporting a mechanosensory or proprioceptive role and no movements were observed when they were fired. It is proposed that peripheral elements utilized in consummatory phases of Aplysia feeding may be directly influenced by a neuronal pathway that is activated during the food-induced arousal state.

Animals↗
PubMed2004

Environmental enrichment results in cortical and subcortical changes in levels of synaptophysin and PSD-95 proteins.

Experience-dependent plasticity is thought to involve selective change in pre-existing brain circuits, involving synaptic plasticity. One model for looking at experience-dependent plasticity is environmental enrichment (EE), where animals are exposed to a complex novel environment. Previous studies using electron microscopy showed that EE resulted in synaptic plasticity in the visual cortex and hippocampus. However, the areas in the brain that have been examined following EE have been limited. The present study quantified potential synaptic plasticity throughout the brains of C57BL/6 mice using an enzyme-linked immunosorbent assay (ELISA) for two synaptic proteins, synaptophysin and PSD-95. EE resulted in increased synaptophysin and PSD-95 levels through major brain regions, including anterior and posterior areas of the forebrain, hippocampus, thalamus, and hypothalamus. However, no changes in synaptophysin were detected in the cerebellum. These results demonstrate that EE results in an increase in levels of both pre- and post-synaptic proteins in multiple regions of the brain, and it is possible that such changes represent the underlying synaptic plasticity occurring in EE.

Adaptation, Physiological↗
PubMed2000

Excitatory role of the hyperpolarization-activated inward current in phasic and tonic firing of rat supraoptic neurons.

The properties and functional roles of the hyperpolarization-activated inward current (I(H)) in magnocellular neurosecretory cells (MNCs) were investigated during sharp microelectrode recordings from supraoptic neurons in superfused explants of rat hypothalamus. Under current clamp, voltage responses to hyperpolarizing current pulses featured depolarizing sags that were abolished by the I(H) blocker ZD 7288. Under voltage clamp, subtraction of current responses to hyperpolarizing steps recorded in the absence and presence of ZD 7288 was used to investigate the properties of I(H). Current-voltage analysis revealed that steady-state I(H) amplitude increases with hyperpolarization, with half-maximal activation of the underlying conductance occurring at -78 mV. The time course of activation of I(H) during hyperpolarizing steps was monoexponential with time constants (100-800 msec) decreasing with hyperpolarization. The effects of ZD 7288 on I(H) were slow (tau, approximately 15 min), irreversible, and half-maximal at 1.8 micrometer. When tested on continuously active MNCs, application of 30-60 micrometer ZD 7288 caused a significant reduction in firing rate. In phasically active MNCs, the drug decreased burst duration and intraburst firing frequency and caused an increase in the duration of interburst intervals. These effects were accompanied with a small hyperpolarization of the membrane potential. In contrast, ZD 7288 had no effect on spike duration, on the amplitude of calcium-dependent afterpotentials, or on the frequencies and amplitudes of spontaneous synaptic potentials. These results confirm the presence of I(H) in MNCs of the rat supraoptic nucleus and suggest that the presence of this conductance provides an excitatory drive that contributes to phasic and tonic firing.

Animals↗
PubMed2002

Interaction between P2Y and NMDA receptors in layer V pyramidal neurons of the rat prefrontal cortex.

In the first part of this study, monosynaptic excitatory postsynaptic potentials (EPSPs) in layer V of the rat prefrontal cortex were evoked by electrical stimulation of layer I. Recordings by intracellular sharp microelectrodes showed that EPSPs were concentration-dependently facilitated by the P2 receptor antagonistic ATP analogue 2-methylthio ATP (2-MeSATP), while ATP itself depressed the synaptic potentials. The inhibitory effect of ATP turned into facilitation in the presence of the adenosine A(1) receptor antagonist DPCPX. The 2-MeSATP-induced potentiation of EPSP amplitudes were prevented by the P2 receptor antagonists PPADS and Suramin. The EPSP was almost abolished by coapplication of the NMDA receptor antagonist AP-5 and the AMPA/kainate receptor antagonist CNQX. After blockade of the NMDA receptor-mediated part of the EPSP by AP-5, the stimulatory effect of 2-MeSATP disappeared. When NMDA or AMPA were pressure-applied onto pyramidal cells, only the NMDA-induced depolarization was potentiated by 2-MeSATP. In the second part of the study, NMDA-induced currents were measured by whole-cell patch-clamp pipettes. ATP, 2-MeSATP, UDP and UTP potentiated the response to NMDA, while ADP-beta-S was inactive. PPADS antagonized the effect of ATP. Synaptic isolation of pyramidal neurons by a Ca(2+)-free medium or tetrodotoxin did not alter the effect of ATP which, however, was markedly depressed when GTP in the micropipette was replaced by GDP-beta-S. These observations suggest that in layer V pyramidal neurons of the prefrontal cortex postsynaptically localized P2Y receptors interact with NMDA receptor-channels.

Adenosine Triphosphate↗
PubMed2000

Seizures accelerate anoxia-induced neuronal death in the neonatal rat hippocampus.

Seizures occurring in infants with hypoxia are frequently associated with an ominous prognosis. There is, however, no direct evidence that seizures are involved in the pathogenesis of hypoxia-induced neuronal damage. Here, we report that seizures significantly aggravate the hypoxic state by accelerating rapid anoxic depolarization (AD) and associated neuronal death in preparations of the intact hippocampus of neonatal rats in vitro. Under control conditions, prolonged episodes of anoxia/aglycemia induced rapid suppression of synaptic activity followed sequentially by brief bursts of epileptiform activity and then by rapid AD. AD was associated with irreversible neuronal damage manifested by irreversible loss of the membrane potential, synaptic responses, and neuronal degeneration. Aggravation of electrographic seizure activity during anoxic episodes by the adenosine A1 receptor antagonists DPCPX and caffeine or the gamma-aminobutyric acid-A receptor antagonist bicuculline or pretreatment with 4-aminopyridine accelerated AD and associated neuronal death by up to twofold, whereas blockade of seizure activity by the glutamate receptor antagonists or tetrodotoxin significantly delayed the onset of AD. This report provides direct evidence for the need to prevent seizures during neonatal brain hypoxia.

Action Potentials↗
PubMed2004

5-HT1A, 5-HT2, and GABAB receptors interact to modulate neurotransmitter release probability in layer 2/3 somatosensory rat cortex as evaluated by the paired pulse protocol.

Activation of gamma-aminobutyric acid B (GABA(B)) and 5-hydroxytryptamine (5-HT) receptors produces presynaptic inhibition at glutamatergic terminals in the rat neocortex. To evaluate interactions between these metabotropic receptors, field potentials were recorded in layer 2/3 of somatosensory cortex. In addition, the paired pulse (PP) protocol was used to measure changes in the ratio of the second/first extracellular synaptic potentials (S(2)/S(1) ratio) as an index of glutamate release probability in the area. Lowering extracellular [Ca(2+)](o) to 0.5 mM, increased the S(2)/S(1) ratio by 318 +/- 134%. 5-HT (1 microM) increased the S(2)/S(1) ratio by 61 +/- 15%. In presence of the GABA(A) antagonist bicuculline (10 microM), 5-HT increased the S(2)/S(1) ratio by 98 +/- 15%. This effect did not desensitize after two consecutive applications of the amine, and was dose dependent in the concentration range between 0.03-1 microM (EC(50) = 2.36 x 10(-7) mol/L). The increase of S(2)/S(1) ratio induced by 5-HT (1 microM) was blocked reversibly by the 5-HT(1A) antagonist NAN-190 (10-30 microM), but was unaffected by the selective GABA(B) antagonist CGP 52432 (1 microM). The action of 5-HT was mimicked by the 5-HT(1A/7) agonist 8OH-DPAT (10 microM), increasing the S(2)/S(1) ratio by 84 +/- 2%, a response that was unaffected by the 5-HT(2/7) antagonist ritanserin (2 microM). The 5-HT(1B) agonist CP93129 (10 microM) had no effect. The GABA(B) agonist baclofen (1 microM) increased the S(2)/S(1) ratio up to 308 +/- 33%, which is similar to that produced by low [Ca(2+)](o). When the effect of baclofen was maximal, application of 5-HT (1 microM) reversed the S(2)/S(1) ratio back to 78 +/- 27%, a result that was blocked by the 5-HT(2/7) antagonist ritanserin (100 nM). Notably, the interaction between the GABA(B) agonist and 5-HT was order dependent, because enhancement of the S(2)/S(1) ratio elicited by baclofen was not inhibited if 5-HT was applied first. These results suggest a complex interaction between GABA(B), 5-HT(1A), and 5-HT(2) receptors in layer 2/3 of rat somatosensory cortex. Activation of GABA(B) receptors induces PP facilitation (inhibits glutamate release) more efficiently than does activation of 5-HT(1A) receptors. When the effect of GABA(B) receptor activation is maximal, however, the influence of 5-HT changes to the opposite direction, inhibiting PP facilitation (increasing glutamate release) through activation of 5-HT(2) receptors.

Animals↗
PubMedDate not supplied

Functional elongation of CA1 hippocampal neurons with aging in Fischer 344 rats.

Dendritic function of CA1 pyramidal cells was measured during intracellular recording in vitro and correlated with in vivo behavior in Fischer 344 rats. The aged rats (greater than 26 months) were significantly impaired on a water maze test of hippocampal behavioral function. CA1 neurons from these aged rats demonstrated an elevated action potential threshold compared to the young rats. Electrotonic length (L, in lambda), calculated independently from physiological transients and electrotonic cell reconstructions, was significantly longer in neurons from aged rats (L = 0.73 +/- 0.02 lambda; mean +/- SEM) than in neurons from young rats (L = 0.66 +/- 0.02 lambda). Analysis of proximal and distal synaptic potentials pointed to a more distal electrotonic siting of all dendritic synapses in the aged neurons. Thus, electrical lengthening of dendrites, alterations in synaptic location and decreased excitability in neurons from aged rats with behavioral impairment may represent an endpoint of neuronal reactive mechanisms in response to the aging process.

Action Potentials↗
PubMed1986

Electrophysiological control of ciliary motor responses in the ctenophore Pleurobrachia.

Prey capture by a tentacle of the ctenophore Pleurobrachia elicits a reversal of beat direction and increase in beat frequency of comb plates in rows adjacent to the catching tentacle (Tamm and Moss 1985). These ciliary motor responses were elicited in intact animals by repetitive electrical stimulation of a tentacle or the midsubtentacular body surface with a suction electrode. An isolated split-comb row preparation allowed stable intracellular recording from comb plate cells during electrically stimulated motor responses of the comb plates, which were imaged by high-speed video microscopy. During normal beating in the absence of electrical stimulation, comb plate cells showed no changes in the resting membrane potential, which was typically about -60 mV. Trains of electrical impulses (5/s, 5 ms duration, at 5-15 V) delivered by an extracellular suction electrode elicited summing facilitating synaptic potentials which gave rise to graded regenerative responses. High K+ artificial seawater caused progressive depolarization of the polster cells which led to volleys of action potentials. Current injection (depolarizing or release from hyperpolarizing current) also elicited regenerative responses; the rate of rise and the peak amplitude were graded with intensity of stimulus current beyond a threshold value of about -40 mV. Increasing levels of subthreshold depolarization were correlated with increasing rates of beating in the normal direction. Action potentials were accompanied by laydown (upward curvature of nonbeating plates), reversed beating at high frequency, and intermediate beat patterns. TEA increased the summed depolarization elicited by pulse train stimulation, as well as the size and duration of the action potentials. TEA-enhanced single action potentials evoked a sudden arrest, laydown and brief bout of reversed beating. Dual electrode impalements showed that cells in the same comb plate ridge experienced similar but not identical electrical activity, even though all of their cilia beat synchronously. The large number of cells making up a comb plate, their highly asymmetric shape, and their complex innervation and electrical characteristics present interesting features of bioelectric control not found in other cilia.

Action Potentials↗
PubMed1993

Synergistic potentiation of glutamate release by arachidonic acid and oleoyl-acetyl-glycerol.

Both the activation of protein kinase C (PKC) and the facilitation of depolarization-evoked glutamate release have been implicated in the induction of hippocampal long-term synaptic potentiation. These observations may be functionally related, since stimulation of PKC activity enhances evoked glutamate release. Recently, it was shown that arachidonic acid and the diacylglycerol analog oleoyl-acetyl-glycerol activate brain PKC in a synergistic fashion. We report the facilitation of depolarization-induced glutamate efflux from hippocampal mossy fiber synaptosomes due to a combination of arachidonic acid and oleoyl-acetyl-glycerol. The potentiating effects appeared to depend on the activation of PKC since they were attenuated by staurosporine. In addition, the effects of arachidonic acid and oleoyl-acetyl-glycerol appeared to be limited to calcium-dependent processes.

Alkaloids↗
PubMed1997

Immunohistochemical and electrophysiological characterization of submucous neurons from the guinea-pig small intestine in organ culture.

Immunohistochemical and electrophysiological properties of submucous neurons were investigated in organ cultures of the guinea-pig small intestine. Preparations of submucosa, with or without the myenteric plexus attached, were maintained in vitro for 3 to 5 days. Immunohistochemical labelling for peptides revealed that the cultured submucous plexus remained substantially intact and the immunoreactivity of cell bodies was well preserved. Substantial sprouting of nerve fibers immunoreactive for vasoactive intestinal peptide (VIP) or neuropeptide Y (NPY) was evident in submucous ganglia after 5 days in organ culture. Nerve fibers immunoreactive for substance P. somatostatin, 5-hydroxytryptamine or tyrosine hydroxylase were substantially depleted in submucous ganglia or perivascular nerves at 3 days and had virtually disappeared after 5 days in cultures of isolated submucosa. During intracellular recording from submucous neurons, action potentials were initiated by depolarizing current pulses in all neurons cultured with or without the myenteric plexus and muscle layers. Electrical stimulation of internodal strands evoked fast excitatory synaptic potentials (fast EPSPs) in nearly all neurons whether or not the myenteric plexus was present during the culture period up to 5 days. The removal of myenteric plexus and extrinsic nerves did not abolish fast EPSPs from submucous neurons, suggesting that some fast EPSPs may originate from neurons in the submucous plexus, although the possibility that new synapses formed by sprouting, or surviving axons severed from myenteric or sympathetic ganglia may have been functional, cannot be entirely excluded. This work demonstrates that the immunohistochemical and electrophysiological characteristics of submucous neurons are largely maintained in organ cultures of the submucosa.

Animals↗