Contextual memory driven by abused drugs such as opiates has a central role in maintenance and relapse of drug-taking behaviors. Although dopamine (DA) signaling favors memory storage and retrieval via regulation of hippocampal-prefrontal connectivity, its role in modulating opiate-associated contextual memory is largely unknown. Here, we report roles of DA signaling within the hippocampal-prefrontal circuit for opiate-related memories. Combining-conditioned place preference (CPP) with molecular analyses, we investigated the DA D1 receptor (D1R) and extracellular signal-regulated kinase (ERK)-cAMP-response element binding protein (CREB) signaling, as well as DA D2 receptor (D2R) and protein kinase B (PKB or Akt)/glycogen synthase kinase 3 (GSK3) signaling in the ventral hippocampus (vHip) and medial prefrontal cortex (mPFC) during the formation of opiate-related associative memories. Morphine-CPP acquisition increased the activity of the D1R-ERK-CREB pathway in both the vHip and mPFC. Morphine-CPP reinstatement was associated with the D2R-mediated hyperactive GSK3 via Akt inhibition in the vHip and PFC. Furthermore, integrated D1R-ERK-CREB and D2R-Akt-GSK3 pathways in the vHip-mPFC circuit are required for the acquisition and retrieval of the morphine contextual memory, respectively. Moreover, blockage of D1R or D2R signaling could alleviate normal Hip-dependent spatial memory. These results suggest that D1R and D2R signaling are differentially involved in the acquisition and retrieval of morphine contextual memory, and DA signaling in the vHip-mPFC connection contributes to morphine-associated and normal memory, largely depending on opiate exposure states.

PurposeWork-related use of information and communication technologies (ICTs) after hours can be potentially detrimental to employee well-being. In the current study, we examine whether psychological detachment mediates the link between work-related use of ICTs after hours and fatigue and whether affective commitment exacerbates this mediated relationship.Design/methodology/approachWe collected two waves of data from 295 employees in Vietnam, with 51% being female and an average age of 37.81 years old (SD = 7.93).FindingsWork-related use of ICTs after hours was positively related to employees' fatigue via psychological detachment. The negative relationship between work-related use of ICTs after hours and psychological detachment was stronger for employees with higher affective commitment.Practical implicationsOrganizations are encouraged to set policies and procedures to reduce work-related use of ICTs after hours to protect employee health; when work-related use of ICTs after hours is necessary, organizations should provide employees, especially those with higher affective commitment, with resources and strategies to better detach from this experience.Originality/valueOur findings contribute to the understanding of how work-related use of ICTs after hours might adversely affect employee well-being through psychological detachment and that more committed employees can be more affected in this process.

This study focuses on the relationships of career calling to job satisfaction in army officers. The direct and indirect (via meaning in life and meaning in work) effects of career calling on job satisfaction were investigated in 355 male army officers in China. For this purpose, structural equation modeling and bootstrap method were used. Results of confirmatory factor analysis verified the latent structures of meaning in work and job satisfaction. Structural equation modeling and χ2 test indicated meaning in work and presence meaning in life partially mediated the association between career calling and job satisfaction. The bootstrap method also revealed a significant indirect path from career calling to job satisfaction through them. These findings extend previous studies and shed light on promoting job satisfaction from a positive and meaningful perspective through the effect of adaptive career calling.

Background:Opiate addiction is associated with complex cognitive impairment, which contributes to the development of compulsive drug use and relapses. Dopamine and N-methyl-D-aspartate receptors play critical roles in opiate-induced cognitive deficits. However, the roles of D1 and D3 receptors in the N-methyl-D-aspartate/glycineB receptor-regulated cognitive behaviors induced by morphine remain unknown.Methods:The 5-choice serial reaction time task was used to investigate the cognitive profiles associated with repeated morphine administration in D1 (D1-/-)- and D3 (D3-/-)-receptor knockout mice. The expression of phosphorylated NR1, Ca2+/calmodulin-dependent protein kinase II (CaMKII), and cAMP response element-binding protein (CREB) in the brain was examined by western blotting. D1-/- and D3-/- mice were treated with the N-methyl-D-aspartate/glycineB site agonist l-aminocyclopropanecarboxylic acid and the antagonist L-701,324 to chronically disrupt N-methyl-D-aspartate receptor function and investigate their effects on morphine-induced cognitive changes.Results:Repeated morphine administration impaired attentional function and caused impulsive and compulsive behaviors. D1-/- mice exhibited hardly any premature nosepokes. D3-/- mice showed robustly increased morphine-induced impulsive behavior. The numbers of premature responses were decreased by L-701,324 administration and increased by ACPC administration; these effects were completely abolished in D1-/- mice due to their inability to perform reward-based tasks. In contrast, the inhibitory effects of L-701,324 on impulsive behavior were significantly augmented in D3-/- mice.Conclusions:N-methyl-D-aspartate/glycineB site functions may contribute to morphine-induced cognitive deficits, especially those related to impulsive behavior. D1 and D3 receptors may have contrasting effects with respect to modulating impulsive behavior. D3 receptors have inhibitory effects on impulsive behaviors, and these effects are clearly mediated by N-methyl-D-aspartate/glycineB receptor and μ-opioid receptor interactions.

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