RESUMO
The trend toward cannabis legalization in the United States over the past two decades has unsurprisingly been accompanied by an increase in the number of cannabis users and use patterns that potentially pose wider risks to the public like driving under the influence. As such, it is becoming increasingly important to develop methods to accurately quantify cannabis intoxication and its associated impairments on cognitive and motor function. Electroencephalography (EEG) offers a non-invasive method for quantitatively assessing neurophysiological biomarkers of intoxication and impairment with a high degree of temporal resolution. Twelve healthy, young recreational cannabis users completed a series of neurocognitive tasks with concurrent EEG acquisition using the ABM STAT X24 EEG headset in a within-subject counterbalanced design. The 1-h testbed consisted of resting state tasks and tests of attention and memory. Spectral densities were computed for resting state tasks, and event-related potentials (ERPs) were obtained for the attention and memory tasks. Theta band power (3-5 Hz) was decreased during cannabis intoxication compared to placebo during resting state tasks, as were average P400 and late positive potential (LPP) amplitudes during attention and memory tasks. Cannabis intoxication was also associated with elevated frontal coherence and diminished anterior-posterior coherence in the Theta frequency band. This work highlights the utility of EEG to identify and quantify neurophysiological biomarkers from recordings obtained during a short neurocognitive testbed as a method for profiling cannabis intoxication. These biomarkers may prove efficacious in distinguishing intoxicated from non-intoxicated individuals in lab and real-world settings.
RESUMO
The central melanocortin system, consisting of melanocortin peptides, agouti gene related peptide and their receptors plays a critical role in the homeostatic control of energy balance. Loss of function mutations in the genes encoding proopiomelanocortin or melanocortin MC(4) receptors cause profound obesity and hyperphagia. However, little is known about the functional relationship of melanocortin neurocircuits to the temporal organization of meal-taking behavior. We used an operant paradigm that combined lever pressing for food pellet deliveries with free water intake monitored by lickometers to quantify meal patterns in mutant mice that selectively lack proopiomelanocortin expression in hypothalamic neurons (nPOMCKO). Compared to wildtype siblings, nPOMCKO mice consumed 50% more food and water daily and exhibited a more stereotyped feeding pattern characterized by reduced inter-meal and inter-mouse variations. Average meals were larger in size but shorter in duration, with no change in meal number. Consequently, intermeal intervals were prolonged in nPOMCKO mice. Similar patterns were observed in pre-obese juvenile and frankly obese adult mice suggesting that neither age nor degree of obesity was responsible for the altered phenotypes. Spontaneous locomotion and wheel running were decreased in nPOMCKO mice, but circadian variations in locomotor and feeding activity were conserved. These data show that hyperphagia in male nPOMCKO mice is due to increased meal size but not meal number, and this pattern is established by age of 5weeks. The combination of larger, more rapidly consumed meals and prolonged intermeal intervals suggests that proopiomelanocortin peptides are necessary for normal meal termination, but not the maintenance of satiety.
