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J Neurophysiol (July 25, 2007). doi:10.1152/jn.00572.2007
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Submitted on May 22, 2007
Accepted on July 20, 2007

Parameter space analysis suggests multi-site plasticity contributes to motor pattern initiation in Tritonia

Robert J Calin-Jageman1*, Mark J Tunstall2, Brett D Mensh3, Paul S. Katz1, and William N. Frost4

1 Biology, Georgia State University, Atlanta, Georgia, United States
2 Neurobiology and Anatomy, University of Texas, Houston, Texas, United States
3 Neuroscience, Columbia University, New York, New York, United States
4 Cell Biology and Anatomy, Rosalind Franklin Univ of Medicine & Science, North Chicago, Illinois, United States

* To whom correspondence should be addressed. E-mail: Rcalinjageman{at}gsu.edu.

This research examines the mechanisms that initiate rhythmic activity in the episodic CPG underlying escape swimming in the gastropod mollusc Tritonia diomedea. Activation of the network is triggered by extrinsic excitatory input but also accompanied by intrinsic neuromodulation and the recruitment of additional excitation into the circuit. To examine how these factors influence circuit activation, a detailed simulation of the unmodulated CPG network was constructed from an extensive set of physiological measurements. In this model, extrinsic input alone is insufficient to initiate rhythmic activity, confirming that multiple processes are involved in circuit activation. However, incorporating known neuromodulatory and polysynaptic effects into the model still failed to enable rhythmic activity, suggesting that additional circuit features are also required. To delineate the additional activation requirements, a large-scale parameter-space analysis was conducted (~2 x 106 configurations). The results suggest that initiation of the swim motor pattern requires substantial reconfiguration at multiple sites within the network, especially to recruit VSI-B activity and increase DSI-C2 coupling. Within the parameter space examined, we observed a tendency for rhythmic activity to be spontaneous and self-sustaining. This suggests that initiation of episodic rhythmic activity may involve temporarily restructuring a non-rhythmic network into a persistent oscillator. In particular, the time course of neuromodulatory effects may control both activation and termination of rhythmic bursting.




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E. S. Hill, A. Sakurai, and P. S. Katz
Transient Enhancement of Spike-Evoked Calcium Signaling by a Serotonergic Interneuron
J Neurophysiol, November 1, 2008; 100(5): 2919 - 2928.
[Abstract] [Full Text] [PDF]




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