Robert E. Hampson

TL;DR: Delta9-Tetrahydrocannabinol from Cannabis sativa is mimicked by cannabimimetic analogs such as CP55940 and WIN55212-2, and antagonized by rimonabant and SR144528, through G-protein-coupled receptors, CB1 in the brain, and CB2 in the immune system.

TL;DR: In vitro autoradiography of agonist-stimulated [35S]GTPγS binding is used to localize cannabinoid receptor-activated G-proteins after chronic Δ9-THC treatment to suggest that profound desensitization of cannabinoid-activated signal transduction mechanisms occurs after chronic cannabinoids treatment.

TL;DR: It is shown that hippocampal neurons in the rat are distributed anatomically in distinct segments along the length of the hippocampus, which represents a structural framework that may help to resolve conflicting views of hippocampal function.

TL;DR: These integrated experimental-modeling studies show for the first time that, with sufficient information about the neural coding of memories, a neural prosthesis capable of real-time diagnosis and manipulation of the encoding process can restore and even enhance cognitive, mnemonic processes.

TL;DR: Investigation of the time course of changes in cannabinoid‐stimulated [35S]GTPγS binding and cannabinoid receptor binding in both brain sections and membranes demonstrated that chronic exposure to ▵9‐THC produced time‐dependent and region‐specific down‐regulation and desensitization of brain cannabinoid receptors, which may represent underlying biochemical mechanisms of tolerance to cannabinoids.