Etienne Hebert-Chatelain

TL;DR: It is shown that the type-1 cannabinoid receptor (CB1) is present at the membranes of mouse neuronal mitochondria, where it directly controls cellular respiration and energy production, revealing a new mechanism of action of G protein–coupled receptor signaling in the brain.

TL;DR: It is shown that acute cannabinoid-induced memory impairment in mice requires activation of hippocampal mtCB1 receptors, and this data reveal that bioenergetic processes are primary acute regulators of cognitive functions.

TL;DR: Positive feedback mediated by pregnenolone reveals a previously unknown paracrine/autocrine loop protecting the brain from CB1 receptor overactivation that could open an unforeseen approach for the treatment of cannabis intoxication and addiction.

TL;DR: In mice, persistent activation of mitochondrial cannabinoid receptors in astroglia impairs cellular glucose metabolism and lactate production, leading to an increase in redox stress in neurons and altered behavioural responses.

TL;DR: The results show that the use of appropriate controls and quantifications allows detecting mtCB1 receptor with CB1 receptor antibodies, and that, if mitochondrial fractions are enriched and purified, CB1 receptors agonists reliably decrease respiration in brain mitochondria, and underline the importance of adapted experimental procedures to study brain mitochondrial functions.