GLR-2 AMPA receptors are required for the npr-1 lethargus defect.

Locomotion behavior of single worms during the L4/A lethargus (A-E and H-J) and in adults (F, K) was analyzed in the indicated genotypes. Instantaneous locomotion velocity (A, H), average motile fraction (B, D, and I), and average locomotion velocity (C, E, F, J and K) are plotted. (A-C) The npr-1 locomotion defect during L4/A lethargus was suppressed by mutations inactivating glr-2 AMPA receptors, and partially reinstated by transgenes expressing GLR-2 in AIA (gcy-28(d) promoter) and DVA (nlp-12 promoter) neurons, but not in Ventral Cord Interneurons (V.C.I., glr-1 promoter) in glr-2;npr-1 double mutants using the indicated promoters. (D-E) glr-1 mutations had no suppressing effect. (F) glr-2 mutations did not block the increased locomotion in npr-1 adults. (G) mEPSCs were recorded from body wall muscles of the adult worms for the indicated genotypes. Summary data are shown. (G) glr-2 mutations did not block the increased mEPSC rate in npr-1 adults. (H-K) Locomotion behavior during the L4/A lethargus (H-J) and in adults (K) of single worms whose DVA neuron is ablated by transgenic overexpression of CED-3 in DVA neuron (nlp-12 promoter) was analyzed in the indicated genotypes. Animals were analyzed by fluorescence microscopy after locomotion recordings to determine if DVA was ablated. The npr-1 locomotion defect during the L4/A lethargus, but not in adults, was partially suppressed in the transgenic animals in which DVA was ablated (-DVA). The number of animals analyzed is indicated for each genotype. Error bars indicate SEM. Values that differ significantly are indicated (**, p <0.01; ***, p <0.001; ns, not significant).