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At least 19 recordsLinked to original sources
PubMed1976

Calcium dependency of excitatory chemical synaptic transmission in the frog cerebellum in vitro.

Chemical synaptic transmission was studied with microelectrode techniques in isolated frog cerebella maintained in vitro. Purkinje cell (PC) EPSPs, elicited by selective monosynaptic electrical stimulation of both the parallel fiber (PF) and climbing fiber (CF) inputs, could be inverted by depolarizing (outward) current injections. Evoked synaptic transmission at both junctions was reduced by lowering the extracellular concentration of calcium ions ([Ca2+]) below 2 mM. Raising [Ca2+] above 2 mM to 8 mM did not further increase synaptic transmission. Mg2+, Sr2+, and Ba2+ did not substitute for Ca2+ in the transmission process.

Animals↗
PubMed1977

The analysis of nonlinear synaptic transmission.

In order to characterize synaptic transmission at a unitary facilitating synapse in the lobster cardiac ganglion, a new nonlinear systems analysis technique for discrete-input systems was developed and applied. From the output of the postsynaptic cell in response to randomly occurring presynaptic nerve impulses, a set of kernels, analogous to Wiener kernels, was computed. The kernels up to third order served to characterize, with reasonable accuracy, the input-output properties of the synapse. A mathematical model of the synapse was also tested with a random impulse train and model predictions were compared with experimental synaptic output. Although the model proved to be even more accurate overall than the kernel characterization, there were slight but consistent errors in the model's performance. These were also reflected as differences between model and experimental kernels. It is concluded that a random train analysis provides a comprehensive and objective comparison between model and experiment and automatically provides an arbitrarily accurate characterization of a system's input-output behavior, even in complicated cases where other approaches are impractical.

Animals↗
PubMed1977

Long-lasting facilitation of synaptic transmission.

After tetanization of several hippocampal pathways (10--50 Hz for 5--15 seconds) there is an increased synaptic transmission of long duration (long-lasting facilitation). The present investigation was undertaken on isolated hippocampal slices to study the mechanism of the effect. The transverse hippocampal slice preparation in vitro allows the simultaneous testing of several afferent fibre systems on the same cell or population of cells. Tetanization of one group of afferent fibres to CA1 pyramids was followed by a long-lasting increase of synaptic transmission along the same fibres, whereas a control input line gave unchanged responses. Using the presynaptic volley as an indicator of the number of afferent impulses, the increased synaptic transmission appeared as an increased excitatory postsynaptic potential (EPSP), increased amplitude and reduced latency of the population spike, and an increased probability of firing of single units. Intracellular recording showed increased EPSPs to afferents of the tetanized line, but no lasting change in membrane resistance or in the response to a depolarizing current pulse. Thus, the effect cannot be ascribed to a general postsynaptic excitability increase. The specific changes in the synaptic transmission may be due either to an increased amount of liberated transmitter or to a local postsynaptic change near the tetanized synapses.

Afferent Pathways↗
PubMed1979

Effects of some divalent cations on synaptic transmission in frog spinal neurones.

1. Synaptic transmission between dorsal root afferents and motoneurones was studied in the isolated and hemisected spinal cord of frogs, using intracellular and extracellular recording techniques, and ionic substitutions of divalent cations in the bathing fluid. 2. Delayed components of excitatory post-synaptic potentials (e.p.s.p.s) evoked in motoneurones by dorsal root supramaximal stimuli, as well as the Ca2+-dependent slow after-hyperpolarization which follows antidromic spikes, were reversibly blocked by superfusing the cords with 'Ca2+-free' media containing Co2+ (4 mM) or Mg2+ (6-10 mM). However, short latency e.p.s.p.s persisted in these media for more than 8 hr. 3. The minimum synaptic delay of the Co2+ and Mg2+, resistant e.p.s.p.s, measured from the peak negativity of the extracellularly recorded presynaptic spike to the onset of the e.p.s.p., was 0.3 msec at 10 +/- 1 degrees C. 4. The Co2+, Mg2+-resistant e.p.s.p.s were graded, and could be elicited by stimulation of segmental or adjacent roots. Those evoked by each of two adjacent roots showed linear summation when the roots were stimulated simultaneously. 5. The Co2+, Mg2+-resistant e.p.s.p.s decreased in amplitude at stimulating frequencies between 10 and 100 Hz, and with paired stimuli at intervals shorter than 20-40 msec. These reductions in amplitude were paralleled by decreases in amplitude of the presynaptic population spike. 6. Solutions free of divalent ions, containing EGTA (2 mM) abolished the Co2+, Mg2+-resistant e.p.s.p.s. They remained blocked for a variable time after returning to Ca2+-free Ringer containing Mg2+ (8 mM). Their continued abolition at this stage is probably not due to changes in electrical properties of motoneuronal membranes. Eventually, the Mg2+-resistant e.p.s.p.s started recovering in the Ca2+-free Ringer containing Mg2+. The time of onset of this recovery depended on the duration of exposure to EGTA. 7. Sr2+ (2-11 mM), although less effective than Ca2+, restored the composite e.p.s.p.s evoked by dorsal root supramaximal stimuli, as well as the Ca2+-dependent slow after-hyperpolarization of the motoneurone. The composite e.p.s.p.s could not be restored with Ba2+ (2-10 mM). 8. The results suggest that the Co2+, Mg2+-resistant e.p.s.p is generated by electrical coupling between some afferent fibres (probably primary afferents) and motoneurones. The after-effects of EGTA treatments probably reflect uncoupling of electrotonic junctions. In contrast, the delayed components of the composite e.p.s.p.s are generated through chemical synapses whose divalent cation requirement is similar to that of the neuromuscular junction.

Action Potentials↗
PubMed1976

Effect of synaptic transmission blockade on morphine action in the guinea-pig myenteric plexus.

Morphine, which inhibits release of acetylcholine from neurons in the myenteric plexus, also inhibits the spontaneous electrical activity of some myenteric neurons. To determine whether morphine acts at a site presynaptic to these neurons, we investigated this morphine effect under conditions of synaptic transmission blockade. Synaptically driven action potentials evoked by point stimulation were recorded extracellularly, and it was shown that all synaptic responses were eliminated or greatly reduced in Ca-free, high-Mg Ringer's with ethylenebis [(oxyethylenenitrilo)]-tetraacetic acid (EGTA), suggesting that synaptic transmission was blocked. Under these conditions, the ability of morphine to inhibit spontaneous electrical activity was virtually unimpaired. Assuming a single locus of narcotic action in the myenteric plexus, it is unlikely, therefore, that the primary action of opiates is to stimulate release of an inhibitory transmitter, to prevent release of an excitatory transmitter or to block the postsynaptic receptor for an excitatory transmitter. Rather, opiates may raise the membrane threshold of a class of neurons. Electric field stimulation activates myenteric neurons, resulting in a morphine-sensitive release of acetylcholine and a contraction of the longitudinal muscle. The ability of field stimulation to induce contractions and of morphine to inhibit these contractions, was virtually unchanged when the only two known excitatory inputs to the cholinergic motor neuron were eliminated by receptor blockade. These observations, taken together, suggest that opiates act directly on the cholinergic motor neuron of the myenteric plexus.

Animals↗
PubMed1979

Synaptic transmission: ion concentration changes in the synaptic cleft.

Currents flowing through the postsynaptic membrane of an active synapse will tend to change the concentrations of ions in the synaptic cleft. Published experimental data are used to predict (a) the sodium and potassium concentration changes in the cleft at the frog neuromuscular junction, and (b) the sodium depletion in the cleft under a Ia synaptic bouton on a cat motoneuron. Significant concentration changes are predicted at both synapses. These changes will contribute to the time dependence of the observed current and will cause the reversal potential of the current to be time dependent. At the frog neuromuscular junction, the time course of the endplate current has been shown previously to depend on the magnitude of the current flowing (at a given potential). We attribute this to changes of the cleft ion concentration. The time dependent changes of the endplate current reversal potential that we predict for the neuromuscular junction are probably too small to be detected. This is because the effects of sodium depletion and potassium accumulation on the reversal potential almost cancel. We predict that near the reversal potential small currents of complex time course will remain, i.e. no true reversl potential exists. Such currents have previously been experimentally. At the cat Ia synapse, the synaptic current is predicted to deplete a significant fraction of the available extracellular sodium ions. Consequently, the magnitude of the synaptic current should be relatively independent of the number of postsynaptic channels activated, and of the membrane potental, as has previously been found experimentally.

Animals↗
PubMed1976

Selective antagonism of frog cerebellar synaptic transmission by manganese and cobalt ions.

Parallel fiber-Purkinje cell synaptic transmission of the frog cerebellum can be selectively blocked by Mn2+ and Co2+. The interaction of these cations with Ca2+ indicates that they act, as has been found for other chemical synapses, at the presynaptic terminals where Ca2+ is required for release of neurotransmitters. Climbing fiber-Purkinje cell synaptic transmission was similarly blocked by Mg2+, Mn2+ and Co2+.

Animals↗
PubMed1977

Depression of synaptic transmission by diphenylhydantoin.

Diphenylhydantoin (phenytoin, DPH) depresses synaptic transmission at the frog neuromuscular synapse by presynaptic and postsynaptic mechanisms. In normal Ringer's solution the amplitude of the neurally evoked end-plate potentials and their quantal content are reduced. Somewhat paradoxically, miniature end-plate potential (mepp) frequency is increased by the drug. These effects could result if DPH blocked both calcium transport at the axonal membrane and intracellular calcium sequestration. Mepp amplitude is reduced, and DPH also induces nerve conduction block at high rates of stimulation. The relevance of these effects to the anticonvulsive activity of DPH is discussed.

Animals↗
PubMed1975

Effects of pressure and anesthetics on conduction and synaptic transmission.

The antagonism observed between pressure and anesthesia in intact animals suggests that pressure antagonism may be a promising criterion for identifying the effects of anesthetics which are important to loss of responsiveness. It is therefore of interest to compare the effects of pressure and anesthesia on conduction and on synaptic transmission, which have often been proposed as possible alternative cellular sites of anesthesia. The model used in this study is the isolated rat superior cervical ganglion. Helium pressure (35-103 atm) antagonized partial conduction block of the preganglionic nerve by halothane(0.5 and 1 mM). Helium pressure failed to antagonize the depressant effects of halothane (0.25-0.5 mM) on nicotinic transmission and of halothane or methoxyflurane (0.24 mM) on muscarinic transmission in the ganglion. Pressure itself severely depressed synaptic transmission and added to the depressant effects of the anesthetics. Conduction block as a possible cellular mechanism of anesthesia therefore meets the proposed criterion of pressure reversibility. In contrast, pressure does not antagonize anesthetic depression of excitatory synaptic transmission in the rat superior cervical ganglion.

Action Potentials↗
PubMed1977

Aspartate and other inhibitors of excitatory synaptic transmission in crayfish muscle.

Synaptic currents were measured in voltage clamped crayfish muscle fibers which were triggered either by stimulation of the motor axon (EPSC), or by L-gutamate (gEPSC) applied by microiontophoresis or superfusion. Among a number of analogues of glutamate, L-glutamic-acid-gamma-methyl ester, L-glutamic-acid-dimethyl ester and L-aspartate, were reasonably specific antagonists at the motor synapses, although at relatively high concentrations. Aslo, 2-amino-4-phosphono-butyric acid and morphine were effective antagonists; the action of morphine, however, seemed to be unspecific. Aspartate was further shown to decrease the size of the quantum EPSC, without affecting the probability of release of transmitter or the potential change recorded from the presynaptic nerve terminal. The results also indicate that aspartate, after longer incubations, is released as a false transmitter. The dose-response curve to short glutamate pulse is shifted by aspartate to higher glutamate concentrations, without affecting the steep slope of the dose-response curve or the saturation level. This effect can be interpreted as competitive inhibition by aspartate, with an equilibrium concentration of aspartate at the receptor of 0.3--1.5 mmol/l. In longer glutamate applications the receptor desensitizes rapidly. Aspartate reduces this desensitization in addition to its competitive inhibitory effect. Suppression of desensitization can be more effective than inhibition in long glutamate applications; in this case aspartate apparently potentiates the effects of glutamate.

Aspartic Acid↗
PubMed1978

Facilitation of synaptic transmission by general anaesthetics.

1. The actions of five structurally different intravenous and inhalation anaesthetics (alphaxalone/alphadolone, halothane, ketamine, methohexitone, and pentobarbitone) have been studied on synaptic transmission through the cuneate nucleus of the dorsal column-lemniscal afferent pathway in the decerebrate cat. 2. Synaptic input and output were estimated from antidromic and orthodromic potentials, which were evoked by either afferent volleys from the periphery or micro-electrode excitation of the presynaptic fibre terminals in the cuneate and recorded at forelimb nerves and the medial lemniscus. 3. Each of the anaesthetic agents potentiated the efficiency of synaptic transmission, as shown by the elevation of input-output curves constructed from the integrals of the potentials evoked by varying intensities of either peripheral or cuneate stimulation. 4. The excitability of the afferent terminals, as measured at the peripheral nerves by the antidromic responses to micro-electrode stimulation, was depressed by the anaesthetics. Post-synaptic excitability, which was assessed from the direct lemniscal response to intra-nuclear stimulation, did not appear to change. 5. Hypotensive states (mean arterial levels less than 60 torr) produced depolarization of presynaptic terminals and depression of synaptic efficiency and transmission; these changes opposed the primary effects of the general anaesthetics. 6. It is concluded that anaesthetics do not depress activity at all synapses of the central nervous system. Their facilitatory action on cuneate transmission is attributed to an enhanced release of excitatory transmitter; the underlying mechanism may be hyperpolarization of the primary afferent terminals, secondary to an increase in K+ conductance.

Alfaxalone Alfadolone Mixture↗
PubMed1979

Effect of delta 9-tetrahydrocannabinol on synaptic transmission in the electric eel electroplaque.

When the innervated membrane of the electric eel electroplaque is exposed to concentrations of delta 9-tetracannabinol of 50 to 100 microM synaptic transmission is blocked in approximately 30 minutes. During the block, the chemosensitivity of the innervated membrane to cholinergic agonists remains unaltered. Direct stimulation of the innervated membrane after synaptic transmission had failed did not elicit any postsynaptic membrane action potentials. The passing of hyperpolarizing currents across the electroplaque caused the nerve terminals which innervate the electroplaque to produce subthreshold potentials which resemble endplate potentials with a prolonged falling phase. With further incubation in the tetrahydrocannabinol solution the subthreshold potentials decreased in size and eventually disappeared. These results indicate that delta 9-tetrahydrocannabinol does not affect the acetylcholine-mediated membrane permeability changes, but instead, reduces the excitability of nonsynaptic membrane of both the pre- and postsynaptic elements.

Action Potentials↗
PubMed1977

Depression of glutamate-mediated synaptic transmission by benzyl alcohol.

The data obtained from this study suggest that the nonionizable anesthetic benzyl alcohol has two prominent actions on GABA- and glutamate-mediated synaptic transmission at the lobster neuromuscular junction. They are as follows: (1) depression of the excitatory end-plate potential and the postsynaptic membrane response to applied glutamate, and (2) a hyperpolarization of the postsynaptic resting membrane potential associated with a decrease in effective membrane resistance. No change in amplitude of the inhibitory end-plate potential or inhibitory reversal potential was seen. Excitatory miniature end-plate potential frequency was also unaffected. The depression of excitatory synaptic transmission appears to be due to a decreased responsiveness of the postsynaptic receptor-ionophore complex.

Action Potentials↗
PubMed1979

Possibly electrotonically-mediated synaptic transmission: time-intensity trades in neurons in the superior olivary complex of cat.

Microelectrode studies were conducted on the probability of firing of neurons in the superior olivary complex of 11 anesthetized cats. Time-intensity trades were established for dichotic clicks. Inhibition was observed for interaural time differences in the region .05--4 msec. The authors point out that these extremely brief times render explanation difficult in terms of chemically-mediate synaptic transmission, and speculate that these results, while of an indirect nature, may be an expression of electrical synaptic transmission.

Animals↗
PubMed1975

Detachment of structurally intact nerve endings from chromatolytic neurones of rat superior cervical ganglion during the depression of synaptic transmission induced by post-ganglionic axotomy.

1. Electrophysiological studies showed that injury of post-ganglionic nerve fibres leads to severe and prolonged depression of synaptic transmission through the rat superior cervical ganglion, beginning within 24 h. This is in line with the results of previous studies in other species and upon other neurones. 2. electron microscopy after post-ganglionic axotomy revealed nerve endings of presynaptic type with all the specialized membrane-related features of a synaptic zone, but which were not apposed to any post-synaptic nervous element. These umusual profiles were interpreted as detached presynaptic nerve endings. In normal and control ganglia, such profiles formed at most 0-5% of all vesicle-containing profiles of presynaptic type; in ganglia with all major post-ganglionic branches cut the proportion rose to approximately 7%, between 3 and 7 d post-operatively. Over this period, the mean incidence of chromatolytic neurones was 74-6%. 3. Concomitantly, the incidence of synapses within the ganglion fell by about 75%, reaching its lowest levels between 3 and 7 d post-operatively. There was strikingly little evidence of persistence of post-synaptic membrane specializations ('membrane thickenings') following detachment of synapses. 4. At longer survival intervals the incidence of synapses gradually increased, and that of detached nerve endings gradually decreased; recovery was well advanced by 42 d. 5. The fall in the incidence of synapses was closely paralleled by a fall in the incidence of desmosome-like attachments in the ganglion; the incidence of such attachments was found to be correlated to a significant degree with that of synapses. 6. It is concluded that most or all of the synapses upon sympathetic neurones become physically dissociated during the chromatolytic reaction of these neurones to axotomy. The failure to persist of ultrastructurally specialized post-synaptic sites, and the loss of desmosomes (particularly marked for those involving purely post-ganglionic nervous elements) suggest that the post-ganglionic neurone is losing all its specializations for attachment. 7. Some evidence suggests that the satellite cells may effect the final separation between pre- and post-synaptic structures.

Action Potentials↗
PubMed1979

Long-lasting synaptic potentials and the modulation of synaptic transmission.

Long-lasting postsynaptic potentials (PSPs) generated by decreases in membrane conductance (permeability) have been reported in many types of neurons. We investigated the possible role of such long-lasting decreases in membrane conductance in the modulation of synaptic transmission in the sympathetic ganglion of the bullfrog. The molecular basis by which such conductance-decrease PSPs are generated was also investigated. Synaptic activation of muscarinic cholinergic receptors on these sympathetic neurons results in the generation of a slow EPSP (excitatory postsynaptic potential), which is accompanied by a decrease in membrane conductance. We found that the conventional "fast" EPSPs were increased in amplitude and duration during the iontophoretic application of methacholine, which activates the muscarinic postsynaptic receptors. A similar result was obtained when a noncholinergic conductance-decrease PSP--the late-slow EPSP--was elicited by stimulation of a separate synaptic pathway. The enhancement of fast EPSP amplitude increased the probability of postsynaptic action potential generation, thus increasing the efficacy of impulse transmission across the synapse. Stimulation of one synaptic pathway is therefore capable of increasing the efficacy of synaptic transmission in a second synaptic pathway by a postsynaptic mechanism. Furthermore, this enhancement of synaptic efficacy is long-lasting by virtue of the long duration of the slow PSP. Biochemical and electrophysiological techniques were used to investigate whether cyclic nucleotides are intracellular second messengers mediating the membrane permeability changes underlying slow-PSP generation. Stimulation of the synaptic inputs, which lead to the generation of the slow-PSPs, increased the ganglionic content of both cyclic AMP and cyclic GMP. However, electrophysiological analysis of the actions of these cyclic nucleotides and the actions of agents that affect their metabolism does not provide support for such a second messenger role for either cyclic nucleotide.

Acetylcholinesterase↗
PubMedDate not supplied

[Model of a neuron-regulator of the effectiveness of synaptic transmission].

In diad and triad synapses of vertebrate retina the transmitter released from one and the same presynaptic membrane can act simultaneously on two (or even three) postsynaptic neurones. The model of such a diad synapse is proposed, in which the positive electrical feed-back is caried out between one of postsynaptic and presynaptic neurones. The feed-back appears because of potential drop across the longitudinal resistance of intercellular gap (RIII) near the activated synapse (see [1]). It is shown that if the input resistance of this postsynaptic neurone (N3) is low (low R3 in fig. 1,), it can operate as a regulator of effectiveness of synaptic transmission between the presynaptic (N1) and the second postsynaptic (N2) neurones. The effectiveness of synpatic transmission (e. g. the steepness of transfer function) is the more, the higher the membrane potential in the neurone acting as a regulator (fig. 2), and the higher the resistance of intercellular gap (RIII) (fig. 2). The model reproduces the effect of polarization of horizontal cells (by means of light or current) on the membrane potential in bipolars of the turtle and fish retina (fig. 3). The analysis of the model also shows that one of the functions of horizontal cells, as regulators of synaptic transmission between photoreceptors and bipolars, may be the detection of small objects and borders of image against uniform background.

Models, Neurological↗
PubMed1976

Synaptic transmission: long-lasting potentiation by a postsynaptic mechanism.

Slow decreases of ionic conductance across neuronal cell membranes, which generate slow synaptic potentials, can increase the effectiveness of synaptic transmission. Slow conductance decreases sufficient magnitude increase the amplitude of monosynaptic fast excitatory postsynaptic potentials in B cells of the bullfrog sympathetic ganglion. By this postsynaptic mechanism, activation of one synaptic pathway can cause an increase in transmission, lasting several minutes, across another synapse. This may provide an important mechanism for synaptic integration and control of neuronal interaction.

Animals↗