Poor inhibitory control predicts sex-specific vulnerability to nicotine rewarding properties in mice.

Rationale: The risk of becoming addicted to tobacco varies greatly from individual to individual, raising the possibility of behavioural biomarkers capable of predicting sensitivity to nicotine reward, a crucial step in the development of nicotine addiction. Amongst all of nicotine's pharmacological properties, one of central importance is the enhancement of cognitive performances, which depend on the balance between attentional processes and inhibitory control. However, whether the cognitive enhancement effects of nicotine are predictive of sensitivity to its rewarding properties is still unknown.

A single mild juvenile TBI in male mice leads to regional brain tissue abnormalities at 12 months of age that correlate with cognitive impairment at the middle age.

Traumatic brain injury (TBI) has the highest incidence amongst the pediatric population and its mild severity represents the most frequent cases. Moderate and severe injuries as well as repetitive mild TBI result in lasting morbidity. However, whether a single mild TBI sustained during childhood can produce long-lasting modifications within the brain is still debated.

Flavor additives facilitate oral self-administration of nicotine solution in mice.

Rationale: Tobacco products are very addictive, partly because they contain nicotine which is reinforcing, but also because they include appealing aromas and tastes. Flavor additives are such sensory stimuli which enhance attractiveness, as well as use and abuse of tobacco and vaping products. Yet, the interaction between these flavor additives and nicotine remains poorly understood.

Double dissociation between actions of dopamine D1 and D2 receptors of the ventral and dorsolateral striatum to produce reinstatement of cocaine seeking behavior.

One of the hallmarks of addiction is the enduring vulnerability to relapse. Following repeated use, cocaine (COC) induces neuroadaptations within the dopamine (DA) system, arguably underlying several aspects of COC-seeking behavior. Peripheral stimulation of D2, but not D1, receptors induces relapse.

Circulating Triglycerides Gate Dopamine-Associated Behaviors through DRD2-Expressing Neurons.

Energy-dense food alters dopaminergic (DA) transmission in the mesocorticolimbic (MCL) system and can promote reward dysfunctions, compulsive feeding, and weight gain. Yet the mechanisms by which nutrients influence the MCL circuitry remain elusive. Here, we show that nutritional triglycerides (TGs), a conserved post-prandial metabolic signature among mammals, can be metabolized within the MCL system and modulate DA-associated behaviors by gating the activity of dopamine receptor subtype 2 (DRD2)-expressing neurons through a mechanism that involves the action of the lipoprotein lipase (LPL).