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. Author manuscript; available in PMC: 2010 Apr 24.
Published in final edited form as: Cell. 2006 Nov 3;127(3):621–633. doi: 10.1016/j.cell.2006.09.035

Figure 5. TRPC channels are required for nicotine-dependent behavior.

Figure 5

(A) 2-APB blocks wild-type animals’ acute response to nicotine. Naïve wild-type animals were assayed on nicotine plates with or without (control) 50 μM 2-APB. *p<0.03 (Mann-Whitney U-test).

(B) Sequence alignment of worm TRP-1 (cTRP-1), worm TRP-2 (cTRP-2), fly TRP (dTRP) and human TRPC3 (hTRPC3). The ankyrin repeats, coil-coil domain, six putative transmembrane domains, and TRP domain are indicated by the underlying dashed brackets, solid brackets, solid lines, and double lines, respectively. (C–D) Gene structure and mutations of trp-1 (C) and trp-2 (D). The positions of the trans-spliced leader sequence (SL1), the first Met and the stop codon are indicated. The underlying hollow rectangle indicates the fragment deleted in the trp-1(sy690) (C) and trp-2(sy691) (D) mutant.

(E) trp-1(sy690) and trp-2(sy691) mutant animals do not respond to acute nicotine treatment. Ex[Pglr-1::trp-2] and Ex[Pglr-1::trp-1] denotes a transgene expressing TRP-2 and TRP-1 under the glr-1 promoter, respectively. See experimental procedures for allele names. *p<0.02 (ANOVA with Kruskal-Wallis H-test). n≥10. Error bars represent SD.