Hye Jean Yoon

TL;DR: Using complementary techniques, it is reported that in vivo recruitment of NAc shell dynorphin neurons, acting through KOR, is necessary and sufficient to drive pain-induced negative affect and provides evidence that pain- induced adaptations in the kappa opioid system within theNAc shell represent a functional target for therapeutic intervention that could circumventPain-induced affective disorders.

TL;DR: The authors found that inflammatory pain decreased the activity of ventral tegmental area (VTA) dopamine (DA) neurons, which are critical mediators of motivational states, and the decreased activity of DA neurons was associated with reduced motivation for natural rewards, consistent with anhedonialike behavior.

TL;DR: In vivo characterization reveals that MP135 maintains untoward side effects such as respiratory depression and reward behavior; together, these results suggest that optimization of MP135 is necessary for the development of therapeutics that suppress the classical side effects associated with conventional clinical opioids.

TL;DR: A population of BNST neurons recruited by α2a-AR signaling that opposes the behavioral action of canonical autoreceptor α2 a-AR populations and which are differentially recruited by distinct stressors is defined and stressor-specific physiological responses in a specific neuronal population are demonstrated.