Browsing by Subject "amygdala"

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    THE NEURAL CORRELATES OF EMOTION REGULATION AND URGENCY
    (Office of the Vice Chancellor for Research, 2012-04-13) Karyadi, Kenny A.; Coskunpinar, Ayca; Cyders, Melissa A.
    Recent studies have indicated five distinct facets of impulsivity related personality traits—each differentially related to risky behaviors. These facets are: sensation seeking, positive and negative urgency, premeditation, and perseverance. Urgency, defined as a tendency to behave impulsively in face of strong emotions, has been found to be the most consistent predictor of a number of problematic risky behaviors—including problematic substance use, pathological gambling, and problematic eating behaviors. It has been theorized that this relationship between urgency and problematic risky be-haviors can be attributed to an underlying dysfunction in the ability to regu-late emotions. No studies have examined the neural correlates of the urgen-cy facets. However, prior studies have looked at the neural correlates of emotion regulation, which is an aspect of the urgency facets. The intention of this poster is to review the neural correlates of emotion regulation in or-der to elucidate the neural mechanisms underlying the urgency facets. Our review of the literature indicates that the amygdala, orbitofrontal cortex, and anterior cingulate cortex are involved in emotion regulation. Particularly, emotion regulation processes may be attributed to the independent and syn-ergistic functioning of these regions. These findings indicate that urgency and possibly other impulsivity related personality traits may have measura-ble neural correlates. Moreover, these findings also introduce the possibility of targeting neural dysfunctions in order to reduce emotionally driven impul-siveness and consequent problematic behaviors.
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    Spared nerve injury differentially alters parabrachial monosynaptic excitatory inputs to molecularly specific neurons in distinct subregions of the central amygdala
    (Wolters Kluwer, 2019-09) Li, Jun-Nan; Sheets, Patrick L.; Pharmacology and Toxicology, School of Medicine
    Dissecting the organization of circuit pathways involved in pain affect is pivotal for understanding behavior associated with noxious sensory inputs. The central nucleus of the amygdala (CeA) comprises distinct populations of inhibitory GABAergic neurons expressing a wide range of molecular markers. CeA circuits are associated with aversive learning and nociceptive responses. The CeA receives nociceptive signals directly from the parabrachial nucleus (PBn), contributing to the affective and emotional aspects of pain. Although the CeA has emerged as an important node in pain processing, key questions remain regarding the specific targeting of PBn inputs to different CeA subregions and cell types. We used a multifaceted approach involving transgenic reporter mice, viral vector-mediated optogenetics, and brain slice electrophysiology to delineate cell-type–specific functional organization of the PBn–CeA pathway. Whole-cell patch clamp recordings of molecularly defined CeA neurons while optogenetically driving long-range inputs originating from PBn revealed the direct monosynaptic excitatory inputs from PBn neurons to 3 major subdivisions of the CeA: laterocapsular (CeC), lateral (CeL), and medial (CeM). Direct monosynaptic excitatory inputs from PBn targeted both somatostatin-expressing (SOM+) and corticotropin-releasing hormone expressing (CRH+) neurons in the CeA. We find that monosynaptic PBn input is preferentially organized to molecularly specific neurons in distinct subdivisions of the CeA. The spared nerve injury model of neuropathic pain differentially altered PBn monosynaptic excitatory input to CeA neurons based on molecular identity and topographical location within the CeA. These results provide insight into the functional organization of affective pain pathways and how they are altered by chronic pain.