Additionally, CaBP overexpression reduced long-term potentiation (LTP), caused a frequency-dependent inhibition of post-tetanic potentiation (PTP), and impaired spatial navigation. Results showed that NAP, at femtomolar concentrations, completely protected against oxygen-glucose deprivation, and cyanide poisoning. View details for Web of Science ID 000168768800002. We hypothesized that psychological morbidity in these conditions may result from gastrointestinal problems, rather than causing them.Functional dyspepsia was induced by neonatal gastric irritation in male rats. Specifically, we show that while the magnitude of hippocampal neuron death caused by the excitotoxin kainic acid is indeed worsened in the presence of GCs, there is no evidence of increased markers of apoptosis. The demonstrated ability of glucocorticoids to cause dendritic expansion and increase excitability in the amygdala could help mediate the behavioral effects of glucocorticoids, and thus may be important therapeutic target for anxiety. View details for Web of Science ID 000317266500023, View details for PubMedCentralID PMC3597033. —Michael Shermer, American Scholar ... Robert M. Sapolsky is the author of several works of nonfiction, including A Primate's Memoir, The Trouble with Testosterone, and Why Zebras Don't Get Ulcers. Ho, D. Y., Mocarski, E. S., Sapolsky, R. M. CORTICOSTERONE IMPAIRS HIPPOCAMPAL NEURONAL CALCIUM REGULATION - POSSIBLE MEDIATING MECHANISMS, ENDOCRINOLOGY ALFRESCO - PSYCHOENDOCRINE STUDIES OF WILD BABOONS, PATTERNS OF ADRENOCORTICOTROPIN SECRETAGOG RELEASE WITH HYPOGLYCEMIA, NOVELTY, AND RESTRAINT AFTER COLCHICINE BLOCKADE OF AXONAL-TRANSPORT. In this review, we briefly consider such progress and how it might be applied to the realm of the aging brain. Most studies have used constitutive vector systems, limiting the ability to control transgene expression in a dose-dependent, time-dependent, or reversible manner. I then review how the stressful characteristics of social rank have adverse adrenocortical, cardiovascular, reproductive, immunological, and neurobiological consequences. 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. Since constitutive expression of a foreign gene or overexpression of an endogenous gene may have deleterious effects, the ability to control temporal expression would be advantageous. A., Dinkel, K. M., Steinberg, G. K., Sapolsky, R. M. Toxoplasma gondii infection induces dendritic retraction in basolateral amygdala accompanied by reduced corticosterone secretion, Treponema pallidum Infection in the Wild Baboons of East Africa: Distribution and Genetic Characterization of the Strains Responsible. We therefore constructed a chimeric gene ("ER/GR") containing the hormone-binding domain of the GC receptor and the DNA binding domain of the estrogen receptor; as a result, ER/GR transduces deleterious GC signals into beneficial estrogenic ones. Increased intracellular calcium accumulation is known to potentiate ischemic injury. The mild hypoglycemia was not in the range which, itself, typically produces hippocampal damage. Hypothermia (33 degrees C) was induced 2 hours after insult and maintained for 3 hours. However, preconditioning and hypothermia block ischemic damage by inhibiting an increase of P-Akt. View details for DOI 10.1016/j.expneurol.2005.02.021, View details for Web of Science ID 000230876100008. Sorrells, S. F., Caso, J. R., Munhoz, C. D., Hu, C. K., Tran, K. V., Miguel, Z. D., Chien, B. Y., Sapolsky, R. M. Derivation of Injury-Responsive Dendritic Cells for Acute Brain Targeting and Therapeutic Protein Delivery in the Stroke-Injured Rat. We investigated these effects by utilizing modified herpes vectors to deliver the anti-apoptotic agents intracerebrally and examined them in the face of excitotoxic and metabolic insults. As a possible explanation for this surprising worsening, CuZnSOD overexpression increased glutathione peroxidase activity in the presence of sodium cyanide but had no effect on catalase or glutathione peroxidase activity in the presence of kainic acid. Overexpression of S6K1 mediated by lentiviral vectors significantly attenuated brain infarction.mTOR plays a crucial protective role in brain damage after stroke and contributes to the protective effects of IPC. This syndrome X-like condition occurred only in the Garbage HL subset. In this study we demonstrate that such vectors can maintain neuronal metabolism and reduce the extent of neuron loss in cultures after a period of hypoglycemia. This lack of clinical protection may result from suboptimal criteria for patient entrance into clinical trials. Taurine concentrations rose after infusion of KA, but were unaffected by GC regime, whereas alanine concentrations were unaffected by either manipulation. In nearly all such studies, however, "protection" consists of reduced neurotoxicity, with no demonstrated preservation of neuronal function. The results clearly show the feasibility of using silicon microphysiometry for assessing metabolism of brain cultures and for exploring the relationship between metabolism and synaptic activation. During post-ischemic reperfusion, reactive oxygen species (ROS) are formed in excess in mitochondria and can play a role in initiating apoptosis. GH is the primary hormone of growth and development and its increase in teenage boys is associated with the adolescent growth spurt. Hypothermia blocked most of these changes and maintained Akt activity. Intact sleep-deprived rats had elevations of circulating Cort, blood, and liver glucose that were absent in intact control and Adx+ animals. During the first two weeks of life rat pups show a markedly reduced adrenocortical response to stress, and this period of adrenocortical quiescence has been termed the 'stress non-responsive period' (SNRP). Davis, A. S., Zhao, H., Sun, G. H., Sapolsky, R. M., Steinberg, G. K. Phosphoinositide-3-kinase/Akt survival signal pathways are implicated in neuronal survival after stroke. Subjects were 51 male Macaca fascicularis monkeys with known behavioral histories and who had been given dexamethasone (DEX) suppression tests a week prior to killing. The rate was proportional to the number of cells and was sensitive to metabolic enhancement or depression. The hypercortisolism found in cases of affective disorders, anorexia nervosa, Alzheimer's disease, among the very aged or the chronically stressed, is not a uniform phenomenon. This is the first demonstration that HSP72 gene transfer even after ischemia onset is neuroprotective. The first involves overexposure of neurons to excitatory N-methyl-D-aspartate (NMDA) receptor agonists, which mobilize damaging concentrations of intracellular calcium; the second involves the generation of damaging tissue acidosis. These results suggest that Cort-induced shifts in GS activity probably do not explain Cort neurotoxicity, although the stress-induced rise in muscle GS may be relevant to certain types of myopathy. Hippocampal neurogenesis and the glycoprotein gp120 of HIV seems to be context dependent as well as the! 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