GLR-2 AMPA receptors are required for the <i>npr-1</i> lethargus defect.

<p>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 <i>npr-1</i> locomotion defect during L4/A lethargus was suppressed by mutations inactivating <i>glr-2</i> AMPA receptors, and partially reinstated by transgenes expressing GLR-2 in AIA (<i>gcy-28(d)</i> promoter) and DVA (<i>nlp-12</i> promoter) neurons, but not in Ventral Cord Interneurons (V.C.I., <i>glr-1</i> promoter) in <i>glr-2;npr-1</i> double mutants using the indicated promoters. (D-E) <i>glr-1</i> mutations had no suppressing effect. (F) <i>glr-2</i> mutations did not block the increased locomotion in <i>npr-1</i> adults. (G) mEPSCs were recorded from body wall muscles of the adult worms for the indicated genotypes. Summary data are shown. (G) <i>glr-2</i> mutations did not block the increased mEPSC rate in <i>npr-1</i> 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 (<i>nlp-12</i> promoter) was analyzed in the indicated genotypes. Animals were analyzed by fluorescence microscopy after locomotion recordings to determine if DVA was ablated. The <i>npr-1</i> 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 (**, <i>p</i> <0.01; ***, <i>p</i> <0.001; ns, not significant).</p>