Stephanie C. Dulawa

Bio: Stephanie C. Dulawa is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Prepulse inhibition & Antidepressant. The author has an hindex of 30, co-authored 56 publications receiving 7925 citations. Previous affiliations of Stephanie C. Dulawa include University of Chicago & Columbia University.

Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants

Abstract: Various chronic antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of antidepressants. These findings suggest that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.

Dopamine D4 Receptor-Knock-Out Mice Exhibit Reduced Exploration of Novel Stimuli

Abstract: The involvement of dopamine neurotransmission in behavioral responses to novelty is suggested by reports that reward is related to increased dopamine activity, that dopamine modulates exploratory behavior in animals, and that Parkinson9s disease patients report diminished responses to novelty Some studies have reported that polymorphisms of the human dopamine D4 receptor (D4R) gene are associated with personality inventory measures of the trait called “novelty-seeking” To explore a potential role for the D4R in behavioral responses to novelty, we evaluated D4R-knock-out (D4R−/−) and wild-type (D4R+/+) mice in three approach–avoidance paradigms: the open field, emergence, and novel object tests These three paradigms differ in the degree to which they elicit approach, or exploratory behavior, and avoidance, or anxiety-related behavior Thus, we used these three tests to determine whether the D4R primarily influences the exploratory or the anxious component of responses to approach–avoidance conflicts D4R−/− mice were significantly less behaviorally responsive to novelty than D4R+/+ mice in all three tests The largest phenotypic differences were observed in the novel object test, which maximizes approach behavior, and the smallest phenotypic differences were found in the open field test, which maximizes avoidance behavior Hence, D4R−/− mice exhibit reductions in behavioral responses to novelty, reflecting a decrease in novelty-related exploration

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

Stress and the brain: from adaptation to disease

Abstract: In response to stress, the brain activates several neuropeptide-secreting systems. This eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators. By targeting many genes, corticosteroids function in a binary fashion, and serve as a master switch in the control of neuronal and network responses that underlie behavioural adaptation. In genetically predisposed individuals, an imbalance in this binary control mechanism can introduce a bias towards stress-related brain disease after adverse experiences. New candidate susceptibility genes that serve as markers for the prediction of vulnerable phenotypes are now being identified.