To establish the relationship between locomotory behavior and dynamics of
neural circuits in the nematode C. elegans we combined molecular and
theoretical approaches. In particular, we quantitatively analyzed the motion of
C. elegans with defective synaptic GABA and acetylcholine transmission,
defective muscle calcium signaling, and defective muscles and cuticle
structures, and compared the data with our systems level circuit model. The
major experimental findings are: (i) anterior-to-posterior gradients of body
bending flex for almost all strains both for forward and backward motion, and
for 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 frequency
on synaptic signaling, and (v) decrease of frequency with increase of the
muscle time constant. Based on (i) we hypothesize that the Central Pattern
Generator (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 the
CPG design if stretch receptor feedback is sufficiently strong and slow. The
model reveals that stretch receptor coupling in the body wall is critical for
generation of the neuromuscular wave. Our model agrees with our behavioral
data(iii), (iv), and (v), and with other pertinent published data, e.g., that
frequency is an increasing function of muscle gap-junction coupling.Comment: Neural control of C. elegans motion with genetic perturbation
