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Itch is an unpleasant sensation that elicits robust scratching and aversive experience. However, the identity of the cells and neural circuits that organize this information remains elusive. Here we show the necessity and sufficiency of chloroquine-activated neurons in the central amygdala (CeA) for both itch sensation and associated aversion. Further, we show that chloroquine-activated CeA neurons play important roles in itch-related comorbidities, including anxiety-like behaviors, but not in some aversive and appetitive behaviors previously ascribed to CeA neurons. RNA-sequencing of chloroquine-activated CeA neurons identified several differentially expressed genes as well as potential key signaling pathways in regulating pruritis. Finally, viral tracing experiments demonstrate that these neurons send projections to the ventral periaqueductal gray that are critical in modulation of itch. These findings reveal a cellular and circuit signature of CeA neurons orchestrating behavioral and affective responses to pruritus in mice.
Learn More >Trigeminal neuralgia, a severe chronic neuropathic pain disorder, is widely believed to be amenable to surgical treatments. Nearly 20% of patients, however, do not have adequate pain relief after surgery. Objective tools for personalized pre-treatment prognostication of pain relief following surgical interventions can minimize unnecessary surgeries and thus are of substantial benefit for patients and clinicians.
Learn More >Low back pain is the most common pain condition seen in primary care, with the most common treatment being analgesic medications, including opioids. A dramatic increase in opioid prescriptions for low back pain over the past few decades has led to increased non-medical use and opioid overdose deaths. Cognitive behavioral therapy (CBT) for chronic pain is an evidence-based non-pharmacological treatment for pain with demonstrated efficacy when delivered using collaborative care models. No previous studies have tested CBT compared to analgesic optimization that includes opioid management in primary care. This paper describes the study design and methods of the CAre Management for the Effective use of Opioids (CAMEO) trial, a 2-arm, randomized comparative effectiveness trial in seven primary care clinics. CAMEO enrolled 261 primary care veterans with chronic (6 months or longer) low back pain of at least moderate severity who were receiving long-term opioid therapy and randomized them to either nurse care management focused on analgesic treatment and optimization (MED) or cognitive behavioral therapy (CBT). All subjects undergo comprehensive outcome assessments at baseline, 3, 6, 9, and 12 months by interviewers blinded to treatment assignment. The primary outcome is pain severity and interference, measured by the Brief Pain Inventory (BPI) total score. Secondary outcomes include health-related quality of life, fatigue, sleep, functional improvement, pain disability, pain beliefs, alcohol and opioid problems, depression, anxiety, and stress.
Learn More >In a previous proof-of-concept study we have demonstrated that visual exposure to specific colors results in pruritic or antipruritic effects.
Learn More >Abdominal pain adversely impacts children with functional gastrointestinal disorders (FGIDs) or organic gastrointestinal disorders (OGIDs); findings are inconsistent regarding diagnosis and health-related quality of life (HRQoL). This study utilizes a positive psychology framework to understand the experience of youth with abdominal pain (i.e., do positive psychological factors, such as optimism and pain self-efficacy, relate to higher HRQoL?). Consistent with a protective factor model of resilience, in which personal assets may serve as buffers between risk factors and negative outcomes, optimism and pain self-efficacy were examined as they relate to HRQoL in youth with abdominal pain. Specifically, exploratory moderational analyses examined a) if optimism and pain self-efficacy moderate the relation between pain and HRQoL, and b) whether diagnostic status moderated the relation between optimism/pain self-efficacy and HRQoL.
Learn More >Chronic pain is conceptualized as a biopsychosocial phenomenon that involves both physical and emotional processes. The vast majority of research regarding these facets of chronic pain characterizes differences between individuals. In this review, we describe problems with assuming that differences between persons accurately characterize within-person processes. We also provide a systematic review of studies that have examined within-person relationships between pain and affect among individuals with chronic pain.
Learn More >This study aimed to explore whether preoperative angiotensin II type 2 receptor (ATR) level in knee osteoarthritis (OA) patients was an independent risk factor for chronic post-surgical pain (CPSP) after total knee arthroplasty (TKA).
Learn More >Peripheral neuropathies in HIV-infected patients are highly debilitating because of neuropathic pain and physical disabilities. We defined prevalence and associated predictive variables for peripheral neuropathy subtypes in a cohort of persons living with HIV (PWH).
Learn More >Opioids play an important role in pain relief, but repeated exposure results in tolerance and dependence. To make opioids more effective and useful, research in the field has focused on reducing the tolerance and dependence for chronic pain relief. Here, we showed the effect of ABIN-1 in modulating morphine function. We used hotplate tests and CPP tests to show that overexpression of ABIN-1 in the mice brain attenuated morphine dependence. These effects of ABIN-1 are most likely mediated through the formation of ABIN-1-β-arrestin2 complexes, which accelerate β-arrestin2 degradation by ubiquitination. With the degradation of β-arrestin2, ABIN-1 overexpression also decreased MOR phosphorylation and internalization following opioid treatment, affecting the β-arrestin2-dependent signaling pathway to regulate morphine tolerance. Importantly, the effect of ABIN-1 on morphine tolerance was abolished in β-arrestin2 knockout mice. Taken together, these results suggest that the interaction between ABIN-1 and β-arrestin2 inhibits MOR internalization to attenuate morphine tolerance, revealing a novel mechanism for MOR regulation. Hence, ABIN-1 may be a therapeutic target to regulate MOR internalization, thus providing a foundation for a novel treatment strategy for alleviating morphine tolerance and dependence. ABIN-1 overexpression in mice brain attenuated morphine tolerance and dependence. The mechanism may be that ABIN-1-β-arrestin-2 complex formation facilitated β-arrestin-2 degradation by ubiquitination. ABIN-1 targeted β-arrestin2 to regulate morphine tolerance Therefore, inhibiting of ABIN-1 is an important strategy to prevent morphine tolerance and dependence.
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