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. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Addict Biol. 2018 Oct 31;25(1):e12691. doi: 10.1111/adb.12691

Figure 4. BulA[T5A;P6O] blockade of physical THC withdrawal responses is not altered by deletion of β2 nAChRs.

Figure 4

(A) BulA[T5A;P6O] (10, 50, 200 pmol/mouse, i.c.v.), a preferred α6β4* nAChR antagonist, dose-dependently reverses the increase of total somatic signs in THC-dependent mice challenged with rimonabant. The injection of BulA[T5A;P6O] (200 pmol/mouse, i.c.v.) by itself or in combination with THC does not affect the total somatic signs compared to vehicle-treated group. ****P < 0.0001 versus vehicle+vehicle+vehicle group; ####P < 0.0001, #P < 0.05 versus THC+rimonabant group. Data reflect mean ± SEM, n=8 mice per group. (B) The effects evoked by the high dose of Bul[T5A;P6O] are not altered in β2 nAChR KO mice. ****P < 0.0001 versus vehicle+vehicle+vehicle respective groups; ####P < 0.0001 versus THC+rimonabant respective groups. Data reflect mean ± SEM, n=7–8 mice per group.