Cognitive and emotional behavior as well as the extracellular level of glutamate in the hippocampus were analyzed at the age of 10-12 weeks old. PolyI:C-treated mice showed anxiety-like behavior, impairment of object recognition memory and social behavior, and sensorimotor gating deficits, as compared to the saline-treated control group. Depolarization-evoked glutamate release in the hippocampus was impaired in polyI:C-treated mice compared to saline-treated control mice. Furthermore, to investigate the
effect of neonatal immune activation Nec-1s molecular weight on the expression levels of schizophrenia-related genes, we analyzed mRNA levels in the hippocampus 2 and 24 h after polyl:C treatment.
No significant differences or only transient and marginal changes were observed between polyl:C-treated and saline-treated control mice in the expression levels of schizophrenia-related genes in the hippocampus. (c) 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Progressive ventricular hypertrophy click here can lead to the development of insulin resistance, a feature of both chronic kidney disease and heart failure. Here we induced uremia in adult male Sprague-Dawley rats using a remnant kidney model and studied the expression of glucose transporters. As expected, the reduction of nephron mass resulted in impaired renal function, cardiac hypertrophy, glucose eFT-508 intolerance, hyperinsulinemia, anemia, and hypertension. Insulin sensitivity was significantly reduced in the uremic animals as determined by oral glucose tolerance tests. After six weeks of uremia, at a point when cardiac hypertrophy had been established, left ventricle tissue had a marked increase in the expression of GLUT4 (insulin-dependent glucose transporter 4), consistent with hypertrophic remodeling,
but not GLUT1 (insulin-independent glucose transporter 1). However, although uremic animals had systemic insulin resistance and glucose intolerance, there was no evidence of impaired GLUT4 translocation in the heart at 6 weeks of uremia, suggesting that other mechanisms may underpin insulin resistance in the uremic heart.”
“We previously found that ginsenoside Rd (GSRd), one of the main active ingredients in Panax Ginseng, attenuates H(2)O(2)-induced oxidative injury in PC12 cells. Mounting evidence suggests that the oxidative stress is crucially involved in the pathophysiologic process of ischemia. In the present study, we examined the protective role of GSRd to attenuate ischemic neuronal injury in vitro. Cultured hippocampal neurons were exposed to oxygen-glucose deprivation (OGD) for 2 h followed by a 24-h reoxygenation.