Stimulation is necessary for the development of tolerance to a neuronal effect of ethanol.

Ethanol accelerates the decay of post-tetanic potentiation at an identified synapse in Aplysia. We have previously shown that with repeated exposures the ethanol effect diminishes, a development termed "tolerance." Here we present evidence that the establishment of tolerance depends on a adequate stimulation of the presynaptic terminal in the presence of ethanol.

Separate serotonin and dopamine receptors modulate the duration of post-tetanic potentiation at an Aplysia synapse without affecting other aspects of synaptic transmission.

We have studied the effect of the biogenic amines, serotonin and dopamine, on post-tetanic potentiation (PTP) at an identified synapse in the abdominal ganglion of Aplysia californica. We found that: (1) 10(-7) M perfused serotonin doubles the rate constant of decay of PTP. The effect is specific in that neither the size of the non-potentiated (isolated) EPSP nor the amplitude of PTP is affected.

Heterosynaptic stimulation modulates the duration of post-tetanic potentiation at an Aplysia synapse without affecting other aspects of synaptic transmission.

Repetitive stimulation of an axon in the right visceropleural connective to the abdominal ganglion of Aplysia californica produces post-tetanic potentiation (PTP) of a unitary monosynaptic EPSP recorded from cell R15. PTP decays within one half hour following cessation of repatitive stimulation. Stimulation of the left visceropleural connective speeds the rate of decay of PTP, but does not affect the amount of potentiation which is developed or the size of the non-potentiated EPSP.

The amplitude of post-tetanic potentiation of the EPSP RC1-R15 in Aplysia is modulated by environmental parameters.

Evidence is presented that the EPSP called RC1-R15, which is recorded from cell R15 of the abdominal ganglion of Aplysia californica upon appropriate stimulation of the right connective, is endogenously active. In previous studies we showed that after repetitive stimulation the amplitude of this EPSP increases and then slowly decays over many minutes, a phenomenon called post-tetanic potentiation (PTP). The rate of endogenous firing of this EPSP varies with time of day and tonicity of the animal's external environment.

Cross-tolerance to effect of ethanol and temperature in Aplysia: preliminary observations.

Reporting an unexpected finding, this article suggests a bidirectional cross-tolerance between ethanol-tolerant and temperature-adapted preparations may be a widespread phenomenon. Further investigation of these findings may provide useful insight into the nature of the specific membrane changes in alcohol tolerance.

Rapid adaptation to neuronal membrane effects of ethanol and low temperature: some speculations on mechanism.

There is increasing evidence that ethanol exerts its primary effect at neuronal membranes by influencing specific lipid--protein or lipid--lipid interactions that control the state of organization of a specific membrane component; for example, a specific lipid--protein complex that controls a particular physiological property. This implies that tolerance to ethanol is the result of a change in the composition and/or state of organization of this critical membrane component. This altered state confers ethanol resistance.

Amplitude and rate of decay of post-tetanic potentiation are controlled by different mechanisms.

Evidence is presented that post-tetanic potentiation (PTP) of the cholinergic, fast, Cl- dependent IPSP seen in cell L5 of the abdominal ganglion of Aplysia californica upon eliciting a spoke in cell L10 is due to an increase in spike-evoked transmitter release. The magnitude of the post-tetanic change in spike-evoked release is inversely correlated with the amount of transmitter released by an isolated presynaptic spike. This was found whether the latter was increased by injection of tetraethyl ammonium (TEA) into the soma of L10 or decreased by hyperpolarization of the soma of L10.

Tolerance to an effect of ethanol on post-tetanic potentiation in Aplysia.

Repetitive electrical stimulation of an identified synapase in the abdominal ganglion of Aplysia californica results in post-tetanic potentiation (PTP) which decays with a single exponential time course. The rate of decay of PTP is accelerated by the initial perfusion of the abdominal ganglion with 0.8 M ethanol in seawater .

Sustained tolerance to a specific effect of ethanol on posttetanic potentiation in Aplysia.

Perfusion with 0.8 molar ethanol in a seawater specifically accelerates the rate of decay of posttetanic potentiation observed after repetitive electrical stimulation of an identified synapse in the abdominal ganglion of Aplysia californica. Repeated perfusion with seawater alternately with and without ethanol leads to a progressive diminution of this specific effect of ethanol, such that after the third application ethanol no longer has any effect on the rate constant of decay of posttetanic poteniation.

Heterosynaptic inhibition modifies the presynaptic plasticities of the transmission process at the synapse in Aplysia californica.

The monosynaptic and unitary excitatory postsynpatic potential (EPSP) observed in cell R15 of the abdominal ganglion of Aplysia californica upon minimal stimulation of the right visceropleural connective exhibits several presynaptic plasticities (synaptic depression, frequency facilitation, post-tetanic potentiation). We studiied effects of branchial nerve stimulation (heterosynaptic stimulation) on these plasticities of the homosynaptic (right connective) path. A burst of heterosynaptic stimulation (20 pulses at 4/sec) decreased the amplitude of an isolated homosynaptic EPSP.

Dopamine, serotonin and related compounds: presynaptic effects on synaptic depression, frequency facilitation, and post-tetanic potentiation at a synapse in Aplysia californica.

Dopamine, serotonin and related compounds (referred to collectively as biogenic amines) were found to modify transmission at the presumably cholinergic synapse made by an axon in the right visceropleural connective onto cell R15 of the abdominal ganglion of Aplysia californica. (1) With chronic application, dopamine hyperpolarizes R15, and serotonin depolarizes R15. Both actions upon the membrane potential desensitize in 10 min.

Frequency facilitation and post-tetanic potentiation of a unitary synaptic potential in Aplysia californica are limited by different processes.

Post-tetanic potentiation (PTP) of the monosynaptic and unitary excitatory postsynaptic potential (EPSP) recorded in cell R15 of the abdominal ganglion of Aplysia californica was observed after repetitive stimulation of the right visceropleural connective. PTP at this synapse developed after a few pulses (about 20) and after trains of low frequency stimulation (1/2 sec) under normal physiological conditions of media and temperature. No phase of post-tetanic depression was observed.

Synaptic depression at a synapse in Aplysia californica: analysis in terms of a material flow model of neurotransmitter.

When a pair of stimuli separated by an appropriate interval is given to the right visceropleural connective of Aplysia californica the amplitude of the second EPSP elicited in cell R15 is usually smaller than the amplitude of the first EPSP. In the present paper we show that this phenomenon, synaptic depression, can be analyzed in terms of the material flow model of neurotransmitter economics developed in our preceding publications. We specifically show how changes in the 4 model parameters; A, the available pool of transmitter; F, the fraction of the available pool released by a presynaptic action potential; M, the rate of transmitter mobilization into the available pool; and D, the rate constant of demobilization of transmitter from the available pool, all effect synaptic depression.

Resting and stimulated values of model parameters governing transmitter release at a synapse in Aplysia californica.

Transmitter release (R) at a synpase in Aplysia californica can be analyzed in terms of a model with the following parameters: A, the available pool of transmitter; F, the fraction of available pool released by a presynaptic action potential; M, the rate of transmitter mobilization into the available pool; D, the rate constant of demobilization of transmitter from the available pool. In the present paper we show that: (1) beginning with an analysis of the recovery from depression of the second of a pair of disolated EPSPs separated by a series of intervals of about 10-60 sec, and assuming that the recovery is due to refilling of a depleted A, it is possible to estimate resting equilibrium values of these parameters; (2) changes in these parameters when a new equilbrium state is reached after prolonged stimulation (e.g.

Cholinergic agents affect two receptors that modulate transmitter release at a central synapse in Aplsia californica.

A unitary, monosynaptic and presumably cholinergic EPSP recorded in cell R15 of the abdominal ganglion of Aplysia californica undergoes depression followed by facilitation when the presynaptic axon is repetitively stimulated at a rate of 1-3 pulses/sec. During trains of stimulation which produced this sequence of phenomena, the effects of a large number of agents known to affect cholinergic transmission in other systems were studied. The agents could be divided into 4 classes: (1) agents having no effect upon transmission at this cholinergic junction; (2) agents of a class typified by curare, which depressed all EPSPs of a train to the same extent, and which are believed to be acting in this system solely as competitive postsynaptic blockers; (3) agents typified by acetylcholine and carbachol (ACh class), which selectively depressed earlier EPSPs of a train more than later EPSPs and which appear to act by reducing the fractional release of transmitter; (4) agents typified by trimethidinium (trimethidinium class), which selectively depress later EPSPs of a train more than earlier EPSPs and which appear to act by reducing the rate of transmitter supply into the readily releasable pool.