ABSTRACT
The current study examined the link between racial-ethnic microaggressions and psychological distress among 308 Asian American (n = 164) and Latinx American (n = 144) college students (54% female). Additionally, coping strategies (engagement and disengagement) were examined as potential mediators in this link. A confirmatory factor analysis (CFA) of the Racial-Ethnic Microaggressions Scale (REMS) was conducted to test the factor structure with an Asian American and Latinx American emerging adult population (Ages 18-26). A multigroup path analysis of the analytic model was then performed to examine the hypothesized relations between racial-ethnic microaggressions, coping strategies, and psychological distress among Asian American and Latinx American participants. Results of the CFA did not support the original 6-factor structure of the REMS in this sample. However, a 1-factor structure (i.e., total scale score) indicated good fit. Findings from the path analysis indicated that among the total sample, racial-ethnic microaggressions were directly linked to increased psychological distress. Furthermore, engagement coping strategies partially mediated this relationship and were linked to less psychological distress. (PsycINFO Database Record
Subject(s)
Adaptation, Psychological , Aggression/psychology , Asian/psychology , Hispanic or Latino/psychology , Mental Health/ethnology , Racism/psychology , Students/psychology , Adaptation, Psychological/physiology , Adolescent , Adult , Aggression/physiology , Ethnicity/psychology , Factor Analysis, Statistical , Female , Humans , Male , Negotiating/psychology , Racial Groups/psychology , United States/ethnology , Young AdultABSTRACT
17ß-estradiol (E2), at high circulating levels, enhances learning and memory in many women, making it a clinical treatment for hormone-related cognitive decline in aging. However, the mechanisms stimulated by E2, which are responsible for its cognitive enhancing effects, remain incompletely defined. Using an ovariectomized rat model, we previously reported that increasing plasma E2 enhances the magnitude of long-term potentiation (LTP) at hippocampal CA3-CA1 synapses, which is caused by a selective increase in current mediated by NR2B-containing NMDARs, leading to an increase in the NMDAR/AMPAR ratio. Whether the increase in NR2B current is causally related to the ability of E2 to enhance hippocampal dependent learning and memory has yet to be tested. Here, we find that E2 enhances performance in the novel object recognition (NOR) task with the same time course we previously showed E2 enhances the LTP magnitude, temporally linking the increase in LTP to enhanced learning and memory. Furthermore, using the selective NR2B subunit antagonist Ro25-6981, we find that the E2-enhanced NOR, like the enhanced LTP, requires hippocampal NR2B-containing NMDARs, specifically in area CA1. Finally, using whole-cell recordings and the phosphatase inhibitor orthovanadate, we investigated whether the E2-induced increase in NMDAR current is caused by an increase in the density of synaptic NMDARs and/or an increase in NMDAR subunit phosphorylation. We find that both mechanisms are responsible for the enhanced NMDAR current in E2-treated rats. Our results show that the E2-enhanced NOR requires a functional increase in NR2B-containing NMDARs, a requirement shared with the E2-enhanced LTP magnitude at CA3-CA1 synapses, supporting the hypothesis that the increase in LTP likely contributes to the enhanced learning and memory following an increase in plasma E2 levels.
