scholarly journals Action-potential duration and the modulation of transmitter release from the sensory neurons of Aplysia in presynaptic facilitation and behavioral sensitization

1986 ◽  
Vol 83 (21) ◽  
pp. 8410-8414 ◽  
Author(s):  
B. Hochner ◽  
M. Klein ◽  
S. Schacher ◽  
E. R. Kandel
Keyword(s):  
Action Potential ◽  
Sensory Neurons ◽  
Action Potential Duration ◽  
Transmitter Release ◽  
Behavioral Sensitization ◽  
Presynaptic Facilitation

Simulation of synaptic depression, posttetanic potentiation, and presynaptic facilitation of synaptic potentials from sensory neurons mediating gill-withdrawal reflex in Aplysia

1985 ◽  
Vol 53 (3) ◽  
pp. 652-669 ◽  
Author(s):  
K. J. Gingrich ◽  
J. H. Byrne
Keyword(s):  
Action Potential ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Transmitter Release ◽  
Neurotransmitter Release ◽  
Synaptic Depression ◽  
Posttetanic Potentiation ◽  
Withdrawal Reflex ◽  
Classic Conditioning ◽  
Presynaptic Facilitation

The defensive gill-withdrawal reflex in Aplysia has proven to be an attractive system for analyzing the neural mechanisms underlying simple forms of learning such as habituation, sensitization, and classic conditioning. Previous studies have shown that habituation is associated with synaptic depression and sensitization with presynaptic facilitation of transmitter release from sensory neurons mediating the reflex. The synaptic depression, in turn, is associated with a decrease in Ca2+ currents in the sensory neurons, whereas presynaptic facilitation with increased Ca2+ currents produced indirectly by a decrease in a novel serotonergic sensitive K+ current. The present work represents an initial quantitative examination of the extent to which these mechanisms account for each of these types of synaptic plasticity. To address these issues a lumped parameter mathematical model of the sensory neuron release process was constructed. Major components of this model include Ca2+-channel inactivation, Ca2+-mediated neurotransmitter release and mobilization, and readily releasable and upstream feeding pools of neurotransmitter. In the model, release of neurotransmitter has a linear function of Ca2+ concentration and is not affected directly by residual Ca2+. The model not only simulates the data of synaptic depression and recovery from depression, but also qualitatively predicts other features of neurotransmitter release that it was not designed to fit. These include features of synaptic depression with high and low levels of transmitter release, posttetanic potentiation, a steep relationship between action potential duration and transmitter release, enhanced release produced by broadening the sensory neuron action potential (presynaptic facilitation), and dramatic synaptic depression with two closely spaced tetraethylammonium (TEA) spikes. The model cannot account fully for synaptic depression with empirically observed somatic Ca2+-current kinetics. Rather a large component of synaptic depression is due to reduction to the pools of releasable neurotransmitter (depletion). In the model when spike durations are greater than 15-20 ms, spike broadening produces little facilitation. However, when spike durations are more physiological, spike broadening leads to enhanced transmitter release.

scholarly journals Activity-dependent enhancement of presynaptic facilitation provides a cellular mechanism for the temporal specificity of classical conditioning in Aplysia.

1994 ◽  
Vol 1 (4) ◽  
pp. 243-257
Author(s):  
G A Clark ◽  
R D Hawkins ◽  
E R Kandel
Keyword(s):  
Action Potential ◽  
Classical Conditioning ◽  
Sensory Neurons ◽  
Cell Activity ◽  
Critical Time ◽  
Ionic Currents ◽  
Temporal Specificity ◽  
The Us ◽  
Activity Dependent ◽  
Presynaptic Facilitation

A hallmark of many forms of classical conditioning is a precise temporal specificity: Learning is optimal when the conditioned stimulus (CS) slightly precedes the unconditioned stimulus (US), but the learning is degraded at longer or backward intervals, consistent with the notion that conditioning involves learning about predictive relationships in the environment. To further examine the cellular mechanisms contributing to the temporal specificity of classical conditioning of the siphon-withdrawal response in Aplysia, we paired action potential activity in siphon sensory neurons (the neural CS) with tail nerve shock (the US) at three critical time points. We found that CS-US pairings at short (0.5 sec) forward intervals produced greater synaptic facilitation at sensorimotor connections than did either 0.5-sec backward pairings or longer (5 sec) forward pairings, as reflected in a differential increase in both the amplitude and rate of rise of the synaptic potential. In the same preparations, forward pairings also differentially reduced the sensory neuron afterhyperpolarization relative to backward pairings, suggesting that changes in synaptic efficacy were accompanied by temporally specific changes in ionic currents in the sensory neurons. Additional experiments demonstrated that short forward pairings of sensory cell activity and restricted applications of the neuromodulatory transmitter serotonin (normally released by the US) differentially enhanced action potential broadening in siphon sensory neurons, relative to backward pairings. Taken together, these results suggest that temporally specific synaptic enhancement engages both spike-width-dependent and spike-width-independent facilitatory processes and that activity-dependent enhancement of presynaptic facilitation may contribute to both the CS-US sequence and proximity requirements of conditioning.

Modulation of Voltage-Activated Calcium Currents by Mechanical Stimulation in Rat Sensory Neurons

1998 ◽  
Vol 80 (4) ◽  
pp. 1647-1652 ◽  
Author(s):  
Yona Bouskila ◽  
Hugh Bostock
Keyword(s):  
Action Potential ◽  
Sensory Neurons ◽  
Mechanical Stimulation ◽  
Action Potential Duration ◽  
Calcium Currents ◽  
Dorsal Root Ganglion Neurons ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Low Threshold ◽  
Ganglion Neurons

Bouskila, Yona and Hugh Bostock. Modulation of voltage-activated calcium currents by mechanical stimulation in rat sensory neurons. J. Neurophysiol. 80: 1647–1652, 1998. We examined the effects of mechanical stress, induced by a stream of bath solution, on evoked action potentials, electrical excitability, and Ca2+ currents in rat dorsal root ganglion neurons in culture with the use of the whole cell patch-clamp technique. Action-potential duration was altered reversibly by flow in 39% of the 51 neurons tested, but membrane potential and excitability were unaffected. The flow-induced increases and decreases in action-potential duration were consistent with the different effects of flow on two types of Ca2+ channel, determined by voltage-clamp recordings of Ba2+ currents. Current through ω-conotoxin–sensitive (N-type) Ca2+ channels increased by an estimated 74% with flow, corresponding to 23% increase in the total high voltage–activated current, whereas current through low-threshold voltage-activated (T-type) channels decreased by 14%. We conclude that modulation of voltage-activated Ca2+ currents constitutes a route by which mechanical events can regulate Ca2+ influx in sensory neurons.

Modulation of Transmitter Release by Action Potential Duration at the Hippocampal CA3-CA1 Synapse

1999 ◽  
Vol 81 (1) ◽  
pp. 288-298 ◽  
Author(s):  
Jing Qian ◽  
Peter Saggau
Keyword(s):  
Action Potential ◽  
Synaptic Transmission ◽  
Action Potential Duration ◽  
Transmitter Release ◽  
Neurotransmitter Release ◽  
Channel Blocker ◽  
Transmission Curve ◽  
Similar Reduction ◽  
Voltage Dependent ◽  
Hippocampal Ca3

Qian, Jing and Peter Saggau. Modulation of transmitter release by action potential duration at the hippocampal CA3-CA1 synapse. J. Neurophysiol. 81: 288–298, 1999. Presynaptic Ca2+ influx through voltage-dependent Ca2+ channels triggers neurotransmitter release. Action potential duration plays a determinant role in the dynamics of presynaptic Ca2+ influx. In this study, the presynaptic Ca2+ influx was optically measured with a low-affinity Ca2+ indicator (Furaptra). The effect of action potential duration on Ca2+ influx and transmitter release was investigated. The K+ channel blocker 4-aminopyridine (4-AP) was applied to broaden the action potential and thereby increase presynaptic Ca2+ influx. This increase of Ca2+ influx appeared to be much less effective in enhancing transmitter release than raising the extracellular Ca2+ concentration. 4-AP did not change the Ca2+ dependence of transmitter release but instead shifted the synaptic transmission curve toward larger total Ca2+ influx. These results suggest that changing the duration of Ca2+ influx is not equivalent to changing its amplitude in locally building up an effective Ca2+ concentration near the Ca2+ sensor of the release machinery. Furthermore, in the presence of 4-AP, the N-type Ca2+ channel blocker ωCgTx GVIA was much less effective in blocking transmitter release. This phenomenon was not simply due to a saturation of the release machinery by the increased overall Ca2+ influx because a similar reduction of Ca2+ influx by application of the nonspecific Ca2+ channel blocker Cd2+ resulted in much more inhibition of transmitter release. Rather, the different potencies of ω-CgTx GVIA and Cd2+ in inhibiting transmitter release suggest that the Ca2+ sensor is possibly located at a distance from a cluster of Ca2+ channels such that it is sensitive to the location of Ca2+ channels within the cluster.

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