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 1,477 records · Page 82Linked to original sources

Evidence that substance P is a neurotransmitter in the myenteric plexus.

Substance P (SP) is an undecapeptide originally isolated from the gut and since shown to occur within neurones in several parts of the peripheral and central nervous systems. Immunohistochemical studies indicate an exceedingly dense network of SP-containing nerves within the myenteric plexus of the guinea pig ileum. These nerves are intrinsic to the gut wall and can release SP to contract the longitudinal muscle layer. We have previously shown that SP directly depolarizes myenteric neurones and that this depolarization has a time course and ionic mechanism similar to the slow excitatory postsynaptic potential (e.p.s.p.) which can be produced by electrical stimulation of presynaptic nerves within the myenteric ganglia. We wondered whether SP might mediate this slow synaptic potential. We report here that the SP depolarization and the slow e.p.s.p. are reversibly depressed by chymotrypsin, an enzyme which degrades SP, although the responses to acetylcholine, serotonin and an unknown hyperpolarizing transmitter are unaffected. The results provide direct evidence that a peptide can mediate chemical transmission between neurones in the mammalian nervous system.

Animals↗

Inhibitory action of Ruthenium red on neuromuscular transmission.

The effect of Ruthenium Red on synaptic transmission was examined at isolated junctions of the frog, by conventional methods for stimulation and intracellular recording. Ruthenium Red (2.5-10.0 muM) reduces the synaptic potential to subthreshold levels. An analysis of this phenomenon shows that the main action of Ruthenium Red is on the presynaptic nerve terminal where it decreases the number of quanta of transmitter liberated by the nerve impulse. It has the following additional effects: a reduction in the amplitude of the spontaneous miniature end plate potentials; an increase in their frequency; and an increase in delayed release of transmitter after a nerve impulse. Some of these results are discussed in terms of the known inhibitory action of Ruthenium Red on calcium transport across mitochondrial membranes.

Calcium↗

Long-term effects of selective target removal on brainstem premotor neurons in the adult cat.

The electrical activity of antidromically identified abducens internuclear neurons selectively deprived of their target motoneurons was recorded in chronic alert cats. Target motoneurons were killed by the injection of the cytotoxic lectin of Ricinus communis into the medial rectus muscle. Following target removal, the discharge pattern of abducens internuclear neurons showed an overall decrease in firing rate, a significant reduction in their sensitivity to eye position and velocity, and the presence of anomalous responses such as bursts of spikes associated with off-directed saccades. The decreased excitability of abducens internuclear neurons correlated well with a marked reduction in the synaptic efficacy of their inputs. Thus, both excitatory and inhibitory synaptic potentials of vestibular origin showed a noticeable decrease in amplitude. The alterations in firing properties and synaptic transmission were only observed during an initial period of 3 weeks following ricin injection. Within 1 month the electrophysiological parameters returned to control values and remained unaltered for 1 year. Retrograde labelling of abducens internuclear neurons revealed that no cell death occurred after target loss. The anterograde axonal labelling of these neurons showed a progressive decrease in the density of their axonal terminals, and no sign of redistribution to other areas was found. These findings indicate that abducens internuclear neurons are not dependent on the presence of their natural target cells, either for the survival or for the maintenance of appropriate physiological signals.

Abducens Nerve↗

The role of 5-hydroxytryptamine as a transmitter between identified leech neurones in culture.

The synthesis, storage, release and synaptic actions of 5-hydroxytryptamine (5-HT or serotonin) were studied in order to characterize the synaptic connexion that develops between pairs of identified neurones dissected from the central nervous system of the leech and maintained in culture. Experiments were made with Retzius cells (which are known to contain 5-HT in vivo) and pressure sensory neurones on which they form chemical synapses in culture. Individual, isolated Retzius cells in culture synthesized [3H]5-HT from either [3H]tryptophan or [3H]5-hydroxytryptophan [( 3H]5-HTP). These cells did not synthesize other putative neurotransmitters, such as acetylcholine, dopamine, octopamine, noradrenaline or gamma-aminobutyric acid from their respective precursors. The monoaminergic character of Retzius cells was also demonstrated by staining with Neutral Red and by histofluorescence. Individual, isolated Retzius cells that had synthesized and accumulated [3H]5-HT released this compound when depolarized. Transmitter release was calcium-dependent and was blocked by magnesium. When incubated with [3H]5-HT and washed, Retzius cells in culture accumulated approximately 100 times more labelled 5-HT than did non-serotonergic cells, and 10 times more than Retzius cell somata acutely isolated from the animal and incubated in vitro. Chlorimipramine, a blocker of 5-HT uptake, decreased the amount of [3H]5-HT accumulated by Retzius cells and also caused a reversible increase in the amplitude of the synaptic response in the pressure sensory cell elicited by stimulation of the Retzius cell. Pressure sensory neurones in culture and in vivo responded to 5-HT focally applied by pressure ejection from a micropipette. Small pulses elicited a small, slow hyperpolarization. This response was due, at least in part, to an increase in chloride conductance and desensitized rapidly. With larger pulses, a larger, faster non-desensitizing depolarization was elicited. Together, these results provide evidence that 5-HT released from Retzius cells could be responsible for the chemical synaptic potentials seen in pressure sensory neurones in culture.

5-Hydroxytryptophan↗

An excitatory pathway through dorsal columns to rubrospinal cells in the cat.

A somaesthetic excitatory pathway to rubrospinal cells, via other than cortico- or cerebello-rubral relays, has been demonstrated in cats, using intracellular recording techniques. After lesions of the rostral part of the cerebral cortex and the cerebellum, electrical stimulation of the contralateral forepaw and low intensity stimulation of the dorsal columns produced excitatory post-synaptic potentials (e.p.s.p.s) in rubrospinal cells, which often reached the threshold for firing bursts of spikes. These somaesthetic e.p.s.p.s are composed of a burst of small elementary e.p.s.p.s which progressively create a depolarization with a long-lasting time course. Evidence has been obtained that the pathway runs through the dorsal columns to reach the red nucleus after a relay. Stimulation applied to the dorsal columns gives rise to the response with very low threshold current, close to 20 microA. Also, the firing pattern of lemniscal fibres to single-shock dorsal column stimulation has been correlated with the time course of excitation of the rubrospinal cells. As calculated from latencies of e.p.s.p.s the conduction velocity in the investigated pathway is over 55 m/s in the peripheral nerve fibres, indicating that thick, myelinated fibres are involved. It is suggested that the fast somaesthetic loop might, via the rubrospinal tract, participate in exploratory motor behaviour and in the adaptation of gait to the environment.

Action Potentials↗

A null mutation for the alpha3 nicotinic acetylcholine (ACh) receptor gene abolishes fast synaptic activity in sympathetic ganglia and reveals that ACh output from developing preganglionic terminals is regulated in an activity-dependent retrograde manner.

In vertebrates, synaptic activity exerts an important influence on the formation of neural circuits, yet our understanding of its role in directing presynaptic and postsynaptic differentiation during synaptogenesis is incomplete. This study investigates how activity influences synaptic differentiation as synapses mature during early postnatal life. Specifically, we ask what happens to presynaptic terminals when synapses develop without functional postsynaptic receptors and without fast synaptic transmission. To address this issue, we investigated cholinergic nicotinic synapses in sympathetic ganglia of mice with a null mutation for the alpha3 nicotinic ACh receptor gene. Disrupting the alpha3 gene completely eliminates fast excitatory synaptic potentials on postganglionic sympathetic neurons, establishing a crucial role for alpha3-containing postsynaptic receptors in synaptic transmission. Interestingly, the preganglionic nerve terminals form morphologically normal synapses with sympathetic neurons, and these synapses persist without activity in postnatal animals. Surprisingly, when stimulating the preganglionic nerve at physiological rates, we discovered a significant decrease in ACh output from the presynaptic terminals in these alpha3(-/-) sympathetic ganglia. We show that this decrease in ACh output from the presynaptic terminals results, in part, from a lack of functional high-affinity choline transporters. We conclude the following: (1) fast synaptic transmission in mammalian SCG requires alpha3 expression; (2) in the absence of activity, the preganglionic nerve forms synapses that appear morphologically normal and persist for several weeks; and (3) to sustain transmitter release, developing presynaptic terminals require an activity-dependent retrograde signal.

Animals↗

Distributed input to the tail-siphon withdrawal circuit in Aplysia from neurons in the J cluster of the cerebral ganglion.

Plasticity in the circuits for the withdrawal reflexes has been correlated with several simple forms of nonassociative and associative learning in Aplysia, and biochemical, biophysical, and molecular mechanisms of plasticity in these circuits have been described. In order to examine network features of this plasticity, we identified and characterized a component of the modulatory circuitry for the tail-siphon withdrawal circuit. Activation of mechanoafferent neurons in the J cluster of the cerebral ganglion produced strong and distributed input to the tail-siphon withdrawal circuit. Stimulation of the J cells led to excitatory and inhibitory effects in the sensory neurons in the pleural ganglion, the tail motor neurons in the pedal ganglion, and several classes of interneurons in the pleural ganglion, including the multifunctional neuron LPI17. Activation of the J cells produced both fast and slow post-synaptic potentials in neurons of the tail-siphon withdrawal circuit. Of particular interest was the ability of the J cells to produce slow EPSPs in the pleural sensory neurons. These slow EPSPs were associated with an increase in the excitability of the sensory neurons, but no effect of the J cells on spike duration in the sensory neurons was observed. The J cells appear to mediate both sensory and modulatory inputs to the circuit for tail withdrawal.

Action Potentials↗

Electrophysiological correlates to the intrinsic optical signal in the rat neocortical slice.

The study sought to further our understanding of the correlation between electrophysiological activity and the intrinsic optical signal (IOS) in neocortical slice by combining imaging of IOS with whole-cell and extracellular electrical recording. Columnar-shaped areas of IOS were evoked with electrical stimulation of the layer VI/white matter border. The distribution of IOS intensities linearly correlated with the distribution of evoked excitatory post-synaptic potential amplitudes (R=0.89). The distribution of field potentials was narrower than the distribution of IOS intensities with significantly smaller amplitude of the normalized field potentials in the edge of the column. The data suggest that in the neocortical slice the IOS at the edge of the evoked column reflects primarily the sub-threshold excitatory synaptic activity.

Action Potentials↗

The nature and origin of calcium-insensitive miniature end-plate potentials at rodent neuromuscular junctions.

1. To study the nature and origin of slow-rising, Ca2+-insensitive miniature end-plate potentials (m.e.p.p.s) in mammalian muscle we used intracellular recording techniques and drugs which block acetylcholine (ACh) synthesis or the uptake of ACh into synaptic vesicles. Slow m.e.p.p.s were induced in vivo by paralysing the extensor digitorum longus muscle of the rat with botulinum toxin type A or in vitro by the application of 4-aminoquinoline to the mouse diaphragm nerve-muscle preparation. 2. Hemicholinium-3, which blocks ACh synthesis, reduced the amplitude of all synaptic potentials including slow m.e.p.p.s, but only if the nerve was stimulated. 3. 2(4-phenylpiperidino)cyclohexanol (AH-5183), which blocks the active uptake of ACh into synaptic vesicles, reduced both the frequency and the amplitude of slow m.e.p.p.s and did so without requiring nerve stimulation. 4. No correlation was observed between the molecular leakage of ACh from the motor nerve and the frequency and amplitude of slow m.e.p.p.s. 5. We conclude that slow m.e.p.p.s are caused by the release of ACh from the nerve terminal, possibly from a small pool of synaptic vesicle-like structures.

Acetylcholine↗

Spontaneous electrical activity and interaction of large and small cells in cardiac ganglion of the crab, Portunus sanguinolentus.

1. Semi-isolated preparations of the nine-celled cardiac ganglion of the crab, Portunus sanguinolentus, were studied electrophysiologically, using simultaneous recording from extracellular and two or three intracellular electrodes. Nine penetrations of small cells were achieved. 2. Three large (80 x 120 micron) cells lie near the anterior end of the 5-mm main trunk; two large and four small (less than 50 micron) cells at the posterior end. Large-cell axons pass along the main trunk and then exit to innervate cardiac muscle; small-cell axons do not leave the ganglion. 3. The semi-isolated ganglion produces spontaneous electrical activity organized into regularly patterned, rhythmic bursts of large- and small-cell impulses recurring at rates of 0.3-0.6/s and lasting 500-800 ms. Small impulse activity commences and ends each burst. Small cells fire trains during the burst, but impulses are not synchronized among them. Large-cell trains are synchronous, are at about one-half the frequency, and have fewer impulses than small-cell trains. 4. Intracellular recordings from small cells show a slow, pacemaker depolarization from a maximum membrane potential of -54 mV leading with only a slight inflection at ca. -50 mV to a depolarized plateau at ca. -40 mV; nonovershooting impulses are superimposed on this but cease before it repolarizes. Impulses, therefore, arise at a site distant from the soma and do not invade it. Deflections suggesting synaptic potentials are not seen. 5. Intracellular recordings from large cells show complex depolarizations corresponding to extracellularly recorded bursts. These represent excitatory postsynaptic potentials (EPSPs) corresponding with individual small-cell impulses, attenuated, non-overshooting spikes, and an underlying slow depolarization; usually no pacemaker depolarization is apparent between bursts. Chemically mediated transmission is probable for the EPSPs because they show delay, increase in amplitude with hyperpolarization, sometimes show facilitation, and are reduced in saline having one-third Ca, 3 x Mg. 6. EPSPs, impulses, and the slow depolarization occur synchronously among the large cells. Potentials recorded from posterior cells are attenuated and slower than those of the anterior cells. This is interpreted to reflect sites of occurrence more distant from the soma in the posterior than in the anterior cells. Impulses do not invade the somata. 7. Intracellular recordings from large-cell axons 4 mm from the soma show overshooting action potentials arising sharply from a base line. EPSPs are absent or highly attenuated and there is little underlying depolarization (less than 2 mV). 8. Current passing with electrodes intracellular to two cells has established directly that all large cells are electrotonically coupled and that an anterior cell and a small cell are coupled. Changes of burst rate during current passing into any large cell indicate that all large cells and small cells are electrotonically coupled. 9...

Animals↗

Hydrostatic pressure reduces synaptic efficiency by inhibiting transmitter release.

The amplitude of post-synaptic potentials at an identified synapse in the Aplysia central nervous system can be modulated by the application of hydrostatic pressure. Postsynaptically controlled functions, including responses to acetylcholine and the time course of decay of the synaptic responses, remain unaffected by compression. In contrast, frequency facilitation and posttetanic potentiation, which result from presynaptic processes, are altered by pressure in a manner similar to that of agents that block transmitter release. It is concluded that pressure reduces synaptic efficiency by interfering with certain presynaptic mechanisms associated with transmitter release.

Acetylcholine↗

Whole cell recordings from respiratory neurons in the medulla of brainstem-spinal cord preparations isolated from newborn rats.

In brainstem-spinal cord preparations isolated from newborn rats, a whole cell recording technique was applied to record membrane potentials of inspiratory (Insp) and pre-inspiratory (Pre-I) neurons in the ventrolateral medulla. Labelling of these respiratory neurons with Lucifer Yellow allowed analysis of their locations and morphology. Intracellular membrane potentials from 25 Insp neurons were recorded. Average resting membrane potential was -49 mV (n = 25) and input resistance was 306 M omega. Insp neurons were classified into three types from the patterns of synaptic potentials. Type I neurons (n = 11) had a high probability of excitatory postsynaptic potentials (EPSPs) in the pre- and post-inspiratory phases. Type II neurons (n = 7) showed abrupt transition to the burst phase from the resting potential level without increased EPSPs in the preinspiratory phase. Type III neurons (n = 7) were hyperpolarized by inhibitory postsynaptic potentials (IPSPs) in the pre- and post-inspiratory phases. These Insp neurons, located in the ventrolateral medulla 80-490 microns from the ventral surface, were 10-30 microns in diameter, and had various soma shapes (pyramidal, spherical or fusiform). Intracellular membrane potentials from 24 Pre-I neurons were recorded. The average resting membrane potential was -45 mV (n = 24), and the input resistance was 320 M omega. Typical Pre-I neurons showed fairly great depolarization accompanied by action potentials during their burst phase and repolarization during the inspiratory phase. Most Pre-I neurons appeared to have a high level of synaptic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Effects of partial unfused contractions of the gastrocnemius medialis muscle on homonymous and synergist motor neurons in cats].

Autogenetic inhibition of homonymous and synergist motoneurones can be elicited by very weak partial twitches of gastrocnemius medialis muscle, but during sustained contractions the amplitude of inhibitory post-synaptic potentials decreases quickly. A similar decrease also occurs during stronger contractions. The mechanism responsible for this decrease is still active in low spinal preparations. Pre-synaptic inhibition of Ib afferent fibres might contribute to this reduction of efficiency in the transmission of Ib afferent inputs to motoneurones.

Animals↗

[The effect of carnosine on synaptic transmission in the frog neuromuscular junction].

The influence of carnosine on quantal content of the e.p.p. of the frog cutaneous pectoris muscle was studied. The e.p.p. quantal content decreased in presence of carnosine (8 mmol/l). Removal of carnosine from the incubation medium potentiated synaptic transmission as compared with its level prior to addition of carnosine to the medium (after-potentiation). Depressant presynaptic action of carnosine did not depend on external Ca+2 concentration or initial level of evoked quantum secretion whereas the after-potentiation only occurred in conditions of decreased Ca+2 concentration in the medium. In the blockade of cyclic nucleotides phosphodiesterase with theophylline, carnosine induced the same effects as in the experiments without theophylline. However, the presence of theophylline in the medium during removal of carnosine prevented the after-potentiation. Possible mechanisms of presynaptic effects of carnosine are discussed.

Animals↗

Spinal distribution of extracellular field potentials generated by electrical stimulation of pudendal and perineal afferents in the cat.

Electrical stimulation of sensory pudendal and superficial perineal nerves evokes focal synaptic potentials produced by activation of spinal neurons in the lumbosacral gray matter in chloralose anesthetized or decerebrate cats. The field potentials evoked by sensory pudendal nerve stimulation were located in medial parts of laminae V and VI, and lamina X in the S1 to S3 spinal segments. The superficial perineal cutaneous field potentials partially overlapped with those produced by the pudendal nerve, but in general were localized more laterally in laminae V and VI. The central latencies of the earliest portion of the field potentials evoked by either sensory pudendal or superficial perineal nerves were less than 0.9 ms suggesting that monosynaptic activation of neurons contributed to the potentials.

Afferent Pathways↗

Calcium-dependent potentials in the mammalian sympathetic neurone.

1. Intracellular recordings from post-ganglionic neurones of the rat superior cervical ganglion revealed two non-synaptic potentials dependent upon Ca2+, a hyperpolarizing afterpotential (h.a.p.) and a tetrodotoxin (TTX)-insensitive spike. 2. The h.a.p. followed regeneration discharge of the membrane potential in normal and TTX-containing Locke solution. 3. The h.a.p. appeared to arise from an increased K+ conductance because it was associated with a decrease in input resistance, reversed at -90 mV, and was proportional in magnitude to the extracellular K+ concentration. 4. Tetraethylammonium (TEA) and 4-aminopyridine (4-AP) apparently antagonized a voltage-sensitive K+ conductance because they broadened the action potential. However, these substances reduced only slightly the peak amplitude and earliest phases of the h.a.p. 5. The TTX-insensitive spike was most apparent when TEA was present and was invariably followed by an h.a.p. with a magnitude proportional to that of the spike. 6. The magnitude of the h.a.p. and the TTX-insensitive spike was directly proportional to the external Ca2+ concentration and was antagonized by Co2+ and Mn2+ in a dose-dependent fashion. 7. In normal Locke solution, Ba2+ antagonized the h.a.p. and allowed the neurone to sustain discharge during prolonged depolarization. In Locke solution containing TTX and TEA, Ba2+ reduced the magnitude of the h.a.p. but greatly increased the duration of the TTX-insensitive spike. 8. The h.a.p. was not significantly affected by altering external Cl- concentration and the TTX-insensitive spike was not reduced by altering external Na+ concentration. 9. It is concluded that the post-ganglionic neurone supports a regenerative Ca2+ conductance mechanism which in turn triggers an increased K+ conductance. The h.a.p. appears to result from outward K+ current in both a Ca2+ and voltage-dependent fashion.

Action Potentials↗

Effects of juxta- and intracellular microinjection of ethanol on trigeminal motoneurons in the chronic cat.

The direct cellular effects of ethanol on trigeminal motoneurons were studied in chronic cats during sleep and wakefulness. Intracellular and extracellular recordings were obtained while simultaneously injecting ethanol microdroplets onto the surface (juxtacellularly) or within the soma (intracellularly) of these motoneurons. Juxtacellular ethanol injection resulted in a suppression of neuronal excitability as well as a reduction in the amplitude of action potentials and monosynaptically-induced excitatory postsynaptic potentials. Intracellular ethanol injection led to a slight increase in excitability (i.e. membrane depolarization); concurrently, however, there was a reduction in the amplitude of spike and synaptic potentials. We conclude that the predominant response of trigeminal motoneurons to the direct application of ethanol entails a dose-dependent reduction in membrane excitability in addition to a depression of excitatory synaptic transmission. This pattern of ethanol action was observed throughout the states of quiet sleep and active sleep as well as when the animal was awake.

Animals↗

Enhanced parallel fiber frequency-following after reduction of postsynaptic activity.

The frequency-following capabilities of the parallel fibers (Pf) of the rat cerebellar cortex were studied in the presence and absence of surround synaptic activity. When synaptic potentials were reduced or eliminated by local superfusion of the cerebellum with calcium antagonists or when they were reduced following a stimulation train, the Pfs showed more reliable frequency-following. Enhancement of synaptic activity with 4-aminopyridine (4-AP) application leads to a decrease in the frequency-following capabilities of the Pfs. When calcium antagonists were added to the 4-AP superfusate the synaptic enhancing effect of 4-AP was obliterated, and the Pfs displayed more reliable frequency-following capabilities. In addition, an extracellular slow potential was monitored and described in relation to the amplitude of the parallel fiber volley. We interpret these results to indicate that changes associated with postsynaptic activity of molecular layer neuronal elements may influence the frequency-following properties of presynaptic elements, i.e. the parallel fibers, possibly via an extracellular pathway.

Aminopyridines↗