The hippocampus (HPC) is known to play an important role in learning, a process dependent on synaptic plasticity; however, the molecular mechanisms underlying this are poorly understood. ⌬FosB is a transcription factor that is induced throughout the brain by chronic exposure to drugs, stress, and variety of other stimuli and regulates synaptic plasticity and behavior in other brain regions, including the nucleus accumbens. We show here that ⌬FosB is also induced in HPC CA1 and DG subfields by spatial learning and novel environmental exposure. The goal of the current study was to examine the role of ⌬FosB in hippocampal-dependent learning and memory and the structural plasticity of HPC synapses. Using viral-mediated gene transfer to silence ⌬FosB transcriptional activity by expressing ⌬JunD (a negative modulator of ⌬FosB transcriptional function) or to overexpress ⌬FosB, we demonstrate that HPC ⌬FosB regulates learning and memory. Specifically, ⌬JunD expression in HPC impaired learning and memory on a battery of hippocampaldependent tasks in mice. Similarly, general ⌬FosB overexpression also impaired learning. ⌬JunD expression in HPC did not affect anxiety or natural reward, but ⌬FosB overexpression induced anxiogenic behaviors, suggesting that ⌬FosB may mediate attentional gating in addition to learning. Finally, we found that overexpression of ⌬FosB increases immature dendritic spines on CA1 pyramidal cells, whereas ⌬JunD reduced the number of immature and mature spine types, indicating that ⌬FosB may exert its behavioral effects through modulation of HPC synaptic function. Together, these results suggest collectively that ⌬FosB plays a significant role in HPC cellular morphology and HPC-dependent learning and memory.

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ObjectiveThis study examined the prevalence and correlates of depressive symptoms in North Korean defectors who have been living in South Korea for more than one year.MethodsWe used questionnaires developed by the authors to collect sociodemographic data in addition to the Center for Epidemiologic Studies Depression Scale (CES-D), the Psychosocial Well-being Index to measure stress, and a social support scale. A total of 367 subjects were included in this study.ResultsThe results showed that 30.5% of the men and 34.7% of the women reported depressive symptoms, and 33.1% of the men and 36.1% of the women exhibited signs of severe distress. Correlates of depressive symptoms were lack of occupation [odds ratio (OR)=2.198, 95% confidence interval (CI), 1.247-3.873], having escaped without family (OR=1.725, 95% CI, 1.006-2.959), and a poor subjective sense of health status (OR=3.111, 95% CI, 1.591-6.085).ConclusionContinuing vocational training and career management, psychological support programs, and intensive physical health services are needed to improve the mental health of this population.

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Trimethyltin (TMT) is an organotin compound with potent neurotoxic effects characterized by neuronal destruction in selective regions, including the hippocampus. Glycogen synthase kinase-3 (GSK-3) regulates many cellular processes, and is implicated in several neurodegenerative disorders. In this study, we evaluated the therapeutic effect of lithium, a selective GSK-3 inhibitor, on the hippocampus of adult C57BL/6 mice with TMT treatment (2.6 mg/kg, intraperitoneal [i.p.]) and on cultured hippocampal neurons (12 days in vitro) with TMT treatment (5 µM). Lithium (50 mg/kg, i.p., 0 and 24 h after TMT injection) significantly attenuated TMT-induced hippocampal cell degeneration, seizure, and memory deficits in mice. In cultured hippocampal neurons, lithium treatment (0–10 mM; 1 h before TMT application) significantly reduced TMT-induced cytotoxicity in a dose-dependent manner. Additionally, the dynamic changes in GSK-3/β-catenin signaling were observed in the mouse hippocampus and cultured hippocampal neurons after TMT treatment with or without lithium. Therefore, lithium inhibited the detrimental effects of TMT on the hippocampal neurons in vivo and in vitro, suggesting involvement of the GSK-3/β-catenin signaling pathway in TMT-induced hippocampal cell degeneration and dysfunction.

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