CNR1 and Parkinson disease: Recent reports including ours show that the activation of TRPV1 by CAP [10, 11, 13] or the CB receptor by CB1/2 agonists [18, 21, 33] can prevent glial activation, oxidative stress, and expression of proinflammatory molecules in vivo in animal models of PD produced by the administration of MPTP, 6-OHDA, and LPS.