Attenuation of Novelty-Induced Hyperactivity of Mice by Cannabidiol and Hippocampal Inhibitory Chemogenetics.

Gene-targeted mice with deficient AMPA receptor GluA1 subunits ( mice) show robust hyperlocomotion in a novel environment, suggesting them to constitute a model for hyperactivity disorders such as mania, schizophrenia and attention deficit hyperactivity disorder. This behavioral alteration has been associated with increased neuronal activation in the hippocampus, and it can be attenuated by chronic treatment with antimanic drugs, such as lithium, valproic acid, and lamotrigine. Now we found that systemic cannabidiol strongly blunted the hyperactivity and the hippocampal c-Fos expression of the mice, while not affecting the wild-type littermate controls.

Dopaminergic-GABAergic interplay and alcohol binge drinking.

The dopamine D receptor (DR), in the nucleus accumbens (NAc), plays an important role in alcohol reward mechanisms. The major neuronal type within the NAc is the GABAergic medium spiny neuron (MSN), whose activity is regulated by dopaminergic inputs. We previously reported that genetic deletion or pharmacological blockade of DR increases GABA α6 subunit in the ventral striatum.