Vu0360172

JF-NP-26 (10 mg/kg, i.p. in 6% DMSO, 6% Tween 80 in saline) and alloswitch-1 (10 mg/kg, i.p. in 20% DMSO, 20% Tween 80 in saline) were kindly provided by Professor Llebaria (IQAC-CSIC, Barcelona, Spain). Lithium chloride was purchased from Sigma-Aldrich (Milan, Italy). VU0360172 [N-cyclobutyl-6-(2-(3-fluorophenyl)ethynyl) pyridine-3-carboxamide] was purchased from Tocris Bioscience (Bristol, United Kingdom).

Thirty minutes after the last behavioral session, all animals were pretreated with lithium chloride (LiCl) (100 mg/kg i.p.) (Sigma-Aldrich, Milan, Italy), a dose that was expected to increase receptor agonist-stimulated InsP formation due to lithium’s ability to inhibit the conversion of InsP into free inositol [34 (link)]. Mice were given PAM VU0360172 (30 mg/kg) or vehicle one hour after being treated with lithium chloride. One hour after drug (VU0360172 or vehicle) injections, mice were killed by decapitation, and the prefrontal cortex, dorsal, and ventral hippocampus were quickly dissected and stored at −80 °C until InsP measurements and western blot analysis (See Figure 1 for the experimental diagram and Figure 2 for a schematic representation of prefrontal cortex dissection). Lithium chloride was dissolved in saline and VU0360172 (Tocris Bioscience, United Kingdom) was dissolved in 10% Tween 80 and adjusted to pH 7.4 with NaOH. Drugs and vehicles were administered i.p. in a volume of 5 mL/kg body weight. The dose used for VU0360172 (30 mg/kg) was selected on the basis of our previous data [31 (link)].