View details for Web of Science ID 000172028600039, View details for Web of Science ID 000168303000005, View details for Web of Science ID 000166234300127. We observed an increased number of newborn neurons incorporated in the dentate gyrus of the hippocampus during the 10-week post-stress recovery phase. We found that gp120 failed to induce expression of hsp70, hsp25 or hsp90 in cortical or hippocampal cultures, under conditions where induction can be demonstrated in response to other insults. View details for Web of Science ID 000177140000005. Furthermore, dichlorofluorescein measurements indicated that there was a significant reduction in the accumulation of oxygen radicals associated with this insult. We report that SK2 overexpression reduced anxiety and stress-induced corticosterone secretion at a systemic level. Despite that, there is increasing evidence that GCs are not uniformly anti-inflammatory in the injured nervous system and, in fact, can be pro-inflammatory. Lee, I., Evans, A. K., Yang, C., Works, M. G., Kumar, V., De Miguel, Z., Manley, N. C., Sapolsky, R. M. Mammalian Target of Rapamycin Cell Signaling Pathway Contributes to the Protective Effects of Ischemic Postconditioning Against Stroke. Acute and chronic immobilization stress differentially altered the expression of numerous miRs in two stress-responsive regions of the rat brain, the hippocampal CA1 region and the central nucleus of the amygdala. This ARE+HRE vector system is advantageous in that it allows the expression of a transgene to be activated not only during hypoxia but also maintained after reperfusion, thus prolonging the transgene expression during an ischemic insult. The subjects were 108 yellow baboons (Papio cynocephalus) that have been under long-term study of Amboseli National Park in Kenya. View details for Web of Science ID A1990DP32700010. View details for Web of Science ID 000175326700002. Finally, we consider some of the implications of a system justification perspective for the study of evolutionary psychology, political behavior, and social change. View details for Web of Science ID A1997XR46700017. Bcl-x(L) was significantly higher in striatal astrocytes than in astrocytes from other brain regions and higher in striatal and hippocampal neurons than in cortical neurons. This suggests that different protective strategies may have different efficacies depending on brain region. Thus, plasticity of BLA neurons is sufficiently sensitive so as to be saturated by a single day of stress. In the absence of insult, overexpression of Kv1.1, but not SK2, reduced baseline excitability in dentate gyrus granule cells. Hypothermia did not inhibit beta-catenin phosphorylation, but it blocked beta-catenin degradation in the ischemic penumbra. Additionally, we demonstrate decrease in dendritic length of neurons of ventrolateral nucleus of hypothalamus, important for reproductive mate-choice and increase in the same in dorsomedial nucleus, important for defensive behavior. We investigated the effects of antioxidant gene therapy on ROS accumulation after exposure to either sodium cyanide, kainic acid or oxygen glucose deprivation (OGD). In contrast, the bulk of studies reporting no increase with age were those in which young subjects had elevated basal glucocorticoid concentrations (perhaps reflecting the method and speed of obtaining the blood sample, the social conditions of the rat housing, and/or the recency with which there was a disturbance in the animal room). By 4 hours into the reperfusion period (5 hours after ischemia onset), delivery of the Bcl-2 vector was no longer protective. Such protection involved reduction in mitochondrially derived superoxide. Thus, GCs can worsen the deleterious effects of gp120 in a system that is more physiologically relevant than the fetal monolayer culture and in a region-specific manner. In addition, there was a significant increase in postdexamethasone cortical concentrations with age (p less than 0.01; r = 0.31). This article suggests a similar cause of the hypercortisolism of social subordinance. Recently, it is becoming increasingly clear that some of genes induced during cerebral ischemia may actually serve to rescue the cell from death. Chaperones, especially the stress inducible Hsp70, have been studied for their potential to protect the brain from ischemic injury. Drawing upon a rodent literature, we will also suggest some models by which this can occur. Pathological anxiety is thought to reflect a maladaptive state characterized by exaggerated fear. This approach allowed us to investigate the effects of spatially restricted overexpression of MR and a negative transdominant GR (TD) in the dentate gyrus (DG) subfield of the hippocampus, on short term and long term spatial memory in animals overexpressing one copy of MR or TD, two copies of MR ("MR/MR"), or one copy of each ("MR/TD"). Infection of hippocampal cultures with Bcl-2 vectors enhanced neuron survivorship after exposure to adriamycin, a potent oxygen radical generator. We demonstrate that 1) T. gondii relies on glutamine for optimal infection, replication and viability, and 2) T. gondii-infected bone marrow-derived dendritic cells (DCs) display both "hypermotility" and "enhanced migration" to an elevated glutamine gradient in vitro. More recent findings suggest a similar phenomenon in the human hippocampus associated with many neuropsychiatric disorders. Increases in cytoplasmic Ca2+ concentration ([Ca2+]i) can lead to neuron death. View details for DOI 10.1523/JNEUROSCI.3163-05.2005, View details for Web of Science ID 000232669300024. When such necrotic neurological insults occur, neurons are not passively buffeted, but instead mobilize a variety of defenses in an attempt to decrease the likelihood of neuron death, or to decrease the harm to neighboring neurons (by decreasing the likelihood of inflammation). Lentiviral vectors expressing constitutively active Akt1 and Akt3 (cAkt1 and cAkt3) were injected into the ischemic cortex. Interestingly, those new neurons were more responsive to subsequent chronic stress, as they showed more of a stress-induced decrease in spine density and branching nodes than in neurons born during a non-stress period. Identical 24-h CORT treatment caused a 13% reduction in glucose uptake in astrocytes and a 38% reduction in glycogen content, without affecting the level of intracellular glucose. As an alternative, we explore the neuroprotective potential of protein therapy, using a fusion protein comprised of the death-suppressing BH4 domain of the Bcl-xL protein and the protein transduction domain of the human immunodeficiency virus Tat protein. During the mid-1980s, half of the males died from tuberculosis; because of circumstances of the outbreak, it was more aggressive males who died, leaving a cohort of atypically unaggressive survivors. View details for DOI 10.1016/j.brainres.2008.01.007, View details for Web of Science ID 000254106400020, View details for PubMedCentralID PMC2350209, View details for Web of Science ID 000252726100863. We examined factors influencing this switch in energetic bias from glucose to lactate in cultured hippocampal neurons, focusing on the effects of the physiological changes in lactate, glucose and adenosine concentrations seen during hypoxia-ischemia. 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