Stretch sensitive neurons generate rhythmic motor patterns during forward movemnt in C. elegans

Abstract

Coordinated voluntary and involuntary movements produce rhythmic motor activities to drive locomotory behaviors of animals. In C. elegans, forward locomotion, which is initiated by contraction and relaxation of head muscles, exhibits the rhythmic motor pattern. However, the neuronal and molecular mechanisms to generate rhythmic motor pattern are not fully understood. Previously, it was shown that ablation of the SMB or SMD neurons caused increased reversal and in addition, SMB ablation increased wave width of sinusoidal movement (Gray et al., 2005). To confirm whether the SMB or SMD neurons function in forward movement, we genetically ablated the SMB or SMD neurons. Either SMB or SMD ablated worms exhibited increased reversal rate compared to wild-type animals. We next found that SMB or SMD exhibited rhythmic calcium transients that were induced by the head bending. To gain further insight into which molecules generate rhythmic calcium transient in SMB, we examined SMB neuronal calcium transients in synaptic transmission mutants including unc-13 (neurotransmitter release regulator), unc-31 (dense-core vesicle fusion activator), or unc-9 (innexin). All three mutants showed normal calcium dynamic in SMB, indicating that the rhythmic calcium influx of SMB is independent of synaptic transmission, and SMB may act as a stretch sensitive/proprioceptive receptor neuron to sense head muscle contraction. To identify the stretch receptor(s) in SMB, we examined expression pattern of 29 TRP and DEG/ENaC channels and found that few genes including unc-8 (DEG/ENaC channel) were expressed in SMB. UNC-8 protein is localized to cell bodies and processes around nerve ring. We also observed that SMB specific unc-8 RNAi causes increased wave width. We are currently analyzing unc-8 mutant phenotypes.