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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: The data indicate that cortical feedback projections to the MOB crucially regulate food intake via CB1 receptor signaling, linking the feeling of hunger to stronger odor processing.

TL;DR: It is demonstrated that stimulation of OSNs produces a biphasic postsynaptic excitatory response in mitral cells, and OSN stimulation triggers a strong and slow feedforward inhibition that shapes the feedforward excitation but leaves unaffected the monosynaptic component.

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.

TL;DR: In conclusion, CB1 receptors in skeletal and myocardial muscles are predominantly localized in mitochondria, and the activation of mtCB1 receptors may participate in the mitochondrial regulation of the oxidative activity probably through the relevant enzymes implicated in the pyruvate metabolism, a main substrate for TCA activity.