A cellular mechanism of classical conditioning in Aplysia: activity-dependent amplification of presynaptic facilitation

Science ◽  
1983 ◽  
Vol 219 (4583) ◽  
pp. 400-405 ◽  
Author(s):  
R. Hawkins ◽  
T. Abrams ◽  
T. Carew ◽  
E. Kandel
Keyword(s):  
Classical Conditioning ◽  
Cellular Mechanism ◽  
Activity Dependent ◽  
Presynaptic Facilitation

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.

scholarly journals Activity-Dependent Presynaptic Facilitation and Hebbian LTP Are Both Required and Interact during Classical Conditioning in Aplysia

Neuron ◽  
2003 ◽  
Vol 37 (1) ◽  
pp. 135-147 ◽  
Author(s):  
Igor Antonov ◽  
Irina Antonova ◽  
Eric R. Kandel ◽  
Robert D. Hawkins
Keyword(s):  
Classical Conditioning ◽  
Activity Dependent ◽  
Presynaptic Facilitation

scholarly journals The Contribution of Activity-Dependent Synaptic Plasticity to Classical Conditioning inAplysia

2001 ◽  
Vol 21 (16) ◽  
pp. 6413-6422 ◽  
Author(s):  
Igor Antonov ◽  
Irina Antonova ◽  
Eric R. Kandel ◽  
Robert D. Hawkins
Keyword(s):  
Synaptic Plasticity ◽  
Classical Conditioning ◽  
Activity Dependent

Activity-Dependent Peptidergic Modulation of the Plateau-Generating Neuron B64 in the Feeding Network of Aplysia

2007 ◽  
Vol 97 (2) ◽  
pp. 1862-1867 ◽  
Author(s):  
Hae-Young Koh ◽  
Klaudiusz R. Weiss
Keyword(s):  
Elevated Temperature ◽  
Cellular Mechanism ◽  
Biophysical Properties ◽  
Motor Programs ◽  
Plateau Potential ◽  
Peptide Release ◽  
Protraction Phase ◽  
Activity Dependent ◽  
Potential Threshold ◽  
Stimulation Of

Many behaviors display various forms of activity-dependent plasticity. An example of such plasticity is the progressive shortening of the duration of protraction phase of feeding responses of Aplysia that occurs when feeding responses are repeatedly elicited. A similar protraction-duration shortening is observed in isolated ganglia of Aplysia when feeding-like motor programs are elicited through a prolonged stimulation of the command-like neuron CBI-2. Here, we investigate a cellular mechanism that may underlie this activity-dependent shortening of protraction duration of feeding motor programs. CBI-2 contains two neuropeptides, CP2 and FCAP. Previous work showed that CP2 shortens protraction duration of CBI-2 elicited programs. We show here that the same is true for FCAP. We also show that both CP2 and FCAP modulated the biophysical properties of a plateau-generating neuron, B64, that plays an important role in terminating the protraction phase of feeding motor programs. We find that prestimulation of CBI-2, as well as superfusion of CP2 and FCAP, lowered the threshold for activation of the plateau potential in B64. The threshold-lowering actions of CBI-2 prestimulation were occluded by superfusion of FCAP and CP2. Furthermore, at elevated temperature, conditions under which peptide release is prevented in Aplysia, prestimulation of CBI-2 does not lower the plateau-potential threshold, whereas superfusion of CP2 and FCAP does. Our findings are consistent with the hypothesis that peptides released from CBI-2 lower the threshold for activation of plateau potential in B64, thereby contributing to the shortening of protraction duration when CBI-2 is repeatedly activated.

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