The observations that global CB1 receptor knockout mice (Ledent, et al 1999; Varvel and Lichtman 2002; Zimmer, et al 1999) or animals treated with CB1 receptor antagonists (Compton, et al 1996; Hampson and Deadwyler 1999; Lichtman and Martin 1996; Mallet and Beninger 1998; Rinaldi-Carmona, et al 1994) are resistant to the effects of Δ9-THC in the tetrad assay or on spatial memory indicates that this receptor is predominantly responsible for the CNS effects of marijuana. Research using conditional knockout mouse lines has revealed that CB1 receptors expressed on discrete neuronal subpopulations control the various effects Δ9-THC (Monory, et al 2007). As discussed above, there appears to be a strong GABAergic component to the memory disruptive effects Δ9-THC. However, GABA does not appear to play an appreciable role in the non-mnemonic effects of cannabinoids. Specifically, Δ9-THC produced full tetrad effects in 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
