mutant mice lacking CB1 receptors on GABAergic neurons (Monory, et al 2007). Likewise, bicucculine did not block the effects of this drug in the tetrad assay (Varvel, et al 2004a). In contrast, mice baring a deletion of the CB1 receptor in principal neurons were resistant to the antinociceptive, cataleptic, and hypothermic effects of Δ9-THC, though the locomotor depressive effects were only partially reduced (Monory, et al 2007). In addition, Δ9-THC-induced hypomotility and hypothermia were reduced in mice lacking CB1 receptors on glutamatergic neurons. It will be of great interest to evaluate the effects of Δ9-THC in these different lines of conditional CB1 (-/-) mice in learning and memory paradigms.
