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Mathematical model of cellular mechanisms contributing to presynaptic facilitation
K J Gingrich1, D A Baxter, J H Byrne
1Department of Anesthesiology, Albany Medical College, NY 12208.
Brain Research Bulletin
|September 1, 1988
Summary
Presynaptic facilitation in Aplysia involves spike broadening and transmitter mobilization. Spike broadening underlies sensitization, while mobilization is crucial for dishabituation in sensory neuron synapses.
Area of Science:
- Neuroscience
- Computational Neuroscience
- Cellular Neuroscience
Background:
- Presynaptic facilitation in Aplysia sensory neurons is key to learning.
- Previous models suggested spike broadening and transmitter mobilization mediate this facilitation.
- The relative contributions of these mechanisms required further investigation.
Purpose of the Study:
- To extend a quantitative model of presynaptic facilitation.
- To incorporate detailed kinetics of Ca2+ channels, Ca2+ diffusion, transmitter release, and postsynaptic potentials (PSP).
- To elucidate the distinct roles of spike broadening and transmitter mobilization.
Main Methods:
- Developed an extended quantitative model of sensory neuron synapses.
- Included detailed descriptions of calcium dynamics and neurotransmitter release processes.
- Analyzed the model's prediction of postsynaptic potential (PSP) shapes.
Main Results:
- The model accurately describes the input-output relationship of sensory neuron synapses.
- Predicted changes in PSP shape based on mobilization and spike broadening.
- Differentiated the mechanisms underlying sensitization and dishabituation analogs.
Conclusions:
- Cellular analogs of sensitization are primarily mediated by spike broadening.
- Cellular analogs of dishabituation critically require transmitter mobilization.
- The extended model provides quantitative insights into the dual mechanisms of presynaptic facilitation.