Background and aims: The aim of the present study was to test the impulsivities and compulsivities of behavioral addictions, including Internet gaming disorder (IGD) and gambling disorder (GD), by directly comparing them with alcohol use disorder (AUD) and a healthy control (HC) group. Methods: We enrolled male patients who were diagnosed with IGD, GD or AUD, with 15 patients per group, as well as 15 HCs. Trait impulsivity was measured using the Barratt Impulsiveness Scale version 11 (BIS-11). The stop-signal test (SST) from the Cambridge Neuro-psychological Test Automated Battery (CANTAB) was used to assess the patients’ abilities to inhibit prepotent responses. Compulsivity was measured using the intra–extra dimensional set shift (IED) test from the CANTAB. The Trail Making Test (TMT) was also used in this study. Results: The IGD and AUD groups scored significantly higher on the BIS-11 as a whole than did the HC group (p = 0.001 and p = 0.001, respectively). The IGD and AUD groups also scored significantly higher on the BIS-11 as a whole than did the GD group (p = 0.006 and p = 0.001, respectively). In addition, the GD group made significantly more errors (p = 0.017 and p = 0.022, respectively) and more individuals failed to achieve criterion on the IED test compared with the IGD and HC groups (p = 0.018 and p = 0.017, respectively). Discussion: These findings may aid in the understanding of not only the differences in categorical aspects between individuals with IGD and GD but also in impulsivity–compulsivity dimensional domains. Conclusion: Additional studies are needed to elucidate the neurocognitive characteristics of behavioral addictive disorders in terms of impulsivity and compulsivity.

KCNMA1 encodes the pore-forming α subunit of the “Big K+” (BK) large conductance calcium and voltage-activated K+ channel. BK channels are widely distributed across tissues, including both excitable and nonexcitable cells. Expression levels are highest in brain and muscle, where BK channels are critical regulators of neuronal excitability and muscle contractility. A global deletion in mouse (KCNMA1−/−) is viable but exhibits pathophysiology in many organ systems. Yet despite the important roles in animal models, the consequences of dysfunctional BK channels in humans are not well characterized. Here, we summarize 16 rare KCNMA1 mutations identified in 37 patients dating back to 2005, with an array of clinically defined pathological phenotypes collectively referred to as “KCNMA1-linked channelopathy.” These mutations encompass gain-of-function (GOF) and loss-of-function (LOF) alterations in BK channel activity, as well as several variants of unknown significance (VUS). Human KCNMA1 mutations are primarily associated with neurological conditions, including seizures, movement disorders, developmental delay, and intellectual disability. Due to the recent identification of additional patients, the spectrum of symptoms associated with KCNMA1 mutations has expanded but remains primarily defined by brain and muscle dysfunction. Emerging evidence suggests the functional BK channel alterations produced by different KCNMA1 alleles may associate with semi-distinct patient symptoms, such as paroxysmal nonkinesigenic dyskinesia (PNKD) with GOF and ataxia with LOF. However, due to the de novo origins for the majority of KCNMA1 mutations identified to date and the phenotypic variability exhibited by patients, additional evidence is required to establish causality in most cases. The symptomatic picture developing from patients with KCNMA1-linked channelopathy highlights the importance of better understanding the roles BK channels play in regulating cell excitability. Establishing causality between KCNMA1-linked BK channel dysfunction and specific patient symptoms may reveal new treatment approaches with the potential to increase therapeutic efficacy over current standard regimens.

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Previous studies have reported associations between aggression and Internet addiction disorder (IAD), which has also been linked with anxiety, depression, and impulsiveness. However, the causal relationship between aggression and IAD has thus far not been clearly demonstrated. This study was designed to (a) examine the association between aggression and IAD and (b) investigate the mediating effects of anxiety, depression, and impulsivity in cases in which IAD predicts aggression or aggression predicts IAD. A total of 714 middle school students in Seoul, South Korea, were asked to provide demographic information and complete the

Current antipsychotic drugs (APDs) show efficacy with positive symptoms, but are limited in treating negative or cognitive features of schizophrenia. Whereas all currently FDA-approved medications target primarily the dopamine D2 receptor (D2R) to inhibit G i/omediated adenylyl cyclase, a recent study has shown that many APDs affect not only G i/o -but they can also influence β-arrestin-(βArr)-mediated signaling. The ability of ligands to differentially affect signaling through these pathways is termed functional selectivity. We have developed ligands that are devoid of D2R-mediated G i/o protein signaling, but are simultaneously partial agonists for D2R/βArr interactions. The purpose of this study was to test the effectiveness of UNC9975 or UNC9994 on schizophrenia-like behaviors in phencyclidinetreated or NR1-knockdown hypoglutamatergic mice. We have found the UNC compounds reduce hyperlocomotion in the open field, restore PPI, improve novel object recognition memory, partially normalize social behavior, decrease conditioned avoidance responding, and elicit a much lower level of catalepsy than haloperidol. These preclinical results suggest that exploitation of functional selectivity may provide unique opportunities to develop drugs with fewer side effects, greater therapeutic selectivity, and enhanced efficacy for treating schizophrenia and related conditions than medications that are currently available.

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