To establish the relationship between locomotory behavior and dynamics ofneural circuits in the nematode C. elegans we combined molecular andtheoretical approaches. In particular, we quantitatively analyzed the motion ofC. elegans with defective synaptic GABA and acetylcholine transmission,defective muscle calcium signaling, and defective muscles and cuticlestructures, and compared the data with our systems level circuit model. Themajor experimental findings are: (i) anterior-to-posterior gradients of bodybending flex for almost all strains both for forward and backward motion, andfor neuronal mutants, also analogous weak gradients of undulatory frequency,(ii) existence of some form of neuromuscular (stretch receptor) feedback, (iii)invariance of neuromuscular wavelength, (iv) biphasic dependence of frequencyon synaptic signaling, and (v) decrease of frequency with increase of themuscle time constant. Based on (i) we hypothesize that the Central PatternGenerator (CPG) is located in the head both for forward and backward motion.Points (i) and (ii) are the starting assumptions for our theoretical model,whose dynamical patterns are qualitatively insensitive to the details of theCPG design if stretch receptor feedback is sufficiently strong and slow. Themodel reveals that stretch receptor coupling in the body wall is critical forgeneration of the neuromuscular wave. Our model agrees with our behavioraldata(iii), (iv), and (v), and with other pertinent published data, e.g., thatfrequency is an increasing function of muscle gap-junction coupling.
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