directed against residues 401 – 473 of the C-terminal of CB1. This antibody is thought to preferentially label CB1 receptors on GABAergic, but not glutamatergic, neurons (Katona et al., 2006, Kawamura et al., 2006, Nyilas et al., 2009). By contrast, a highly sensitive later-generation CB1 antibody, raised in guinea pig, detects CB1 receptors on glutamatergic axons in the hippocampus and spinal cord (Katona et al., 2006, Kawamura et al., 2006, Nyilas et al., 2009) that were previously unrecognized by earlier generations of CB1 antibodies (Katona et al., 1999, Egertova and Elphick, 2000, Farquhar-Smith et al., 2000, Salio et al., 2002). Second, immunoreactive labeling by C-terminal antibodies may be masked by the presence of C-terminal interacting proteins (e.g. CRIP1a) that modulate CB1 receptor activity (Niehaus et al., 2007). Third, sensitivity of immunostaining may vary with the level of tissue fixation and receptor internalization (Hohmann, 2002). Fourth, the anatomical divisions of the caudate putamen evaluated also differed between the two studies. One or all of these factors may contribute to differences observed between the previous (Malone et al., 2008) and present report.
