Inflammatory pain modifies reward preferences from larger delayed to smaller immediate rewards in male rats.

Self-control underlies goal-directed behavior in both humans and rodents. The ability to balance immediate and delayed gratification is essential for fine-tuning decision-making processes to achieve optimal rewards. Although delayed gratification has been extensively studied using human neuropsychological assessments, brain imaging techniques, and preclinical research, the impact of chronic pain on these processes remains poorly understood.

Orbitostriatal encoding of reward delayed gratification and impulsivity in chronic pain.

Central robust network functional rearrangement is a characteristic of several neurological conditions, including chronic pain. Preclinical and clinical studies have shown the importance of pain-induced dysfunction in both orbitofrontal cortex (OFC) and nucleus accumbens (NAc) brain regions for the emergence of cognitive deficits. Outcome information processing recruits the orbitostriatal circuitry, a pivotal pathway regarding context-dependent reward value encoding.

Dynamics of Lateral Habenula-Ventral Tegmental Area Microcircuit on Pain-Related Cognitive Dysfunctions.

Chronic pain is a health problem that affects the ability to work and perform other activities, and it generally worsens over time. Understanding the complex pain interaction with brain circuits could help predict which patients are at risk of developing central dysfunctions. Increasing evidence from preclinical and clinical studies suggests that aberrant activity of the lateral habenula (LHb) is associated with depressive symptoms characterized by excessive negative focus, leading to high-level cognitive dysfunctions.

Role of Glutamatergic Projections from Lateral Habenula to Ventral Tegmental Area in Inflammatory Pain-Related Spatial Working Memory Deficits.

The lateral habenula (LHb) and the ventral tegmental area (VTA), which form interconnected circuits, have important roles in the crucial control of sensory and cognitive motifs. Signaling in the LHb-VTA pathway can be exacerbated during pain conditions by a hyperactivity of LHb glutamatergic neurons to inhibit local VTA DAergic cells. However, it is still unclear whether and how this circuit is endogenously engaged in pain-related cognitive dysfunctions.