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Respiratory pattern generator model using Ca++-induced Ca++ release in neurons shows both pacemaker and reciprocal
W L Dunin-Barkowski1, A L Escobar, A T Lovering
1Department of Physiology, Texas Tech University Health Sciences Center, Lubbock, TX 79430-6551, USA. witali.duninbarkowski@ttuhsc.edu
Biological Cybernetics
|November 8, 2003
Summary
This study unifies respiratory rhythm generation models by simulating intracellular calcium dynamics and inhibitory synaptic interactions. Computer models demonstrate how these mechanisms can produce both pacemaker and network-based respiratory rhythms.
Area of Science:
- Neuroscience
- Computational Biology
- Respiratory Physiology
Background:
- Central respiratory rhythmogenesis has two main theories: reciprocal inhibition between neural centers and individual neuron bursting pacemaker activity.
- Hybrid models attempt to reconcile these conflicting mechanisms for respiratory rhythm generation.
Purpose of the Study:
- To demonstrate a unified mechanism for respiratory rhythmogenesis using computer simulations.
- To reconcile existing contradictory models of respiratory rhythm generation.
Main Methods:
- Utilized computer simulations incorporating intracellular calcium dynamics (Ca(++)-dependent K+ channels and Ca(++)-induced Ca++ release).
- Modeled interactions between uncoupled neurons with conditional pacemaker properties and inhibitory synaptic connections between neural pools.
Main Results:
- Simulations showed that intracellular mechanisms confer conditional pacemaker properties to neurons under steady excitatory input.
- Increasing inhibitory synaptic connections between neural pools led to synchronized bursting and eventually reciprocal rhythmic activity.
Conclusions:
- A unified mechanism for respiratory rhythm generation, encompassing both pacemaker and network interactions, is proposed.
- Intracellular calcium dynamics and inhibitory synaptic strength are key factors in determining respiratory rhythm patterns.