RESUMO
Life stress modulates decision making, particularly in the face of risk, in some cases prompting vulnerable populations to make suboptimal, life-altering choices. In the brain, stress is known to alter the extracellular release of catecholamines in structures such as basolateral amygdala (BLA) and nucleus accumbens (NAc). To study the role of catecholamines in risky decision-making in rats, we combined a touch screen task, systemic neuropharmacological manipulation, and direct measurement of norepinephrine (NE) and dopamine (DA) release using fiber photometry. Long-Evans rats were trained on an operant touchscreen decision-making task in which they chose between a safe stimulus that delivered a certain 50µl sucrose, or a risky stimulus that delivered either a 'loss' (10µl sucrose 75% of the time) or 'win' (170µl sucrose 25% of the time). Following the pharmacological induction of stress by administration of the inverse GABAA agonist, FG7142, rats were biased in their decisions towards safe choices and the avoidance of loss. This exaggerated loss aversion was blocked by co-treatment with the a2A receptor antagonist, yohimbine. Direct optical measurement of NE release in the BLA and DA release in the NAc revealed temporal dynamics time-locked to the task events and directly related to the outcome of each trial. In both structures, pharmacological stress altered catecholamine release, with systemic yohimbine showing opposing modulation. These findings highlight the catecholamine basis of loss aversion and neuromodulation of critical brain structures during stress.
RESUMO
The thalamic reticular nucleus (TRN) is crucial for the modulation of sleep-related oscillations. The caudal and rostral subpopulations of the TRN exert diverse activities, which arise from their interconnectivity with all thalamic nuclei, as well as other brain regions. Despite the recent characterization of the functional and genetic heterogeneity of the TRN, the implications of this heterogeneity for sleep regulation have not been assessed. Here, using a combination of optogenetics and electrophysiology in C57BL/6 mice, we demonstrate that caudal and rostral TRN modulations are associated with changes in cortical alpha and delta oscillations and have distinct effects on sleep stability. Tonic silencing of the rostral TRN elongates sleep episodes, while tonic silencing of the caudal TRN fragments sleep. Overall, we show evidence of distinct roles exerted by the rostral and caudal TRN in sleep regulation and oscillatory activity.
