Figure 4.

The neural circuit underlying navigation regulates the aversive response to osmotic upshifts. A, Inhibiting the activity of the interneurons AIB and AIY by expressing twk-18(gf) produces significant defects in generating an increased turning rate in response to the osmotic upshift from 150 to 400 mOsm. n = 40 and 38 transgenic animals expressing twk-18(gf) in AIB and AIY were tested in 150 and 400 mOsm, respectively; and n = 40 and 38 WT sibling animals were tested in 150 and 400 mOsm, respectively. B, Inhibiting AIB, AIY, and AIZ by expressing twk-18(gf) produces significant defects in generating an increased turning rate in response to the osmotic upshift from 150 to 400 mOsm. n = 40 and 33 transgenic animals expressing twk-18(gf) in AIB, AIY, and AIZ were tested in 150 and 400 mOsm, respectively; n = 40 and 39 WT sibling animals were tested in 150 and 400 mOsm, respectively. C, Blocking the neural transmission of several command interneurons and motor neurons by expressing the tetanus toxin with the glr-1 promoter produces significant defects in generating an increased turning rate in response to the osmotic upshift from 150 to 400 mOsm. n = 24 animals in all conditions. D, Blocking the neural transmission of several motor neurons by expressing the tetanus toxin with the lad-2 promoter produces significant defects in generating an increased turning rate in response to the osmotic upshift from 150 to 400 mOsm. n = 23 transgenic animals expressing the tetanus toxin with the lad-2 promoter were tested in either 150 or 400 mOsm; and n = 22 and 23 WT sibling animals were tested in 150 and 400 mOsm, respectively. For all, animals are cultivated on the standard NGM plates with an osmotic condition of 150 mOsm, and the significant interaction between genotype (transgenic vs nontransgenic siblings) and osmolarity is tested using two-way ANOVA, ***p < 0.001, **p < 0.01. Values are reported as the mean ± SEM. WT, wild type.