(3) After repeated morphine administration, naloxone precipitation induced significant abstinent jumping in wild-type mice, whereas naloxone-induced abstinent jumping was not observed in AQP4 knockout mice. This suggested that AQP4 deficiency
inhibited the development of morphine physical dependence. (4) Repeated morphine administration clown-regulated cerebral glutamate transporter I (GLT-1) expression in wild-type mice. However, the clown-regulation of GLT-1 expression diminished in AQP4 knockout mice. Taken together, these results demonstrated that AQP4 deficiency potentiated morphine analgesia, attenuated morphine tolerance and physical dependence. The suppression of down-regulation of cerebral GLT1 expression might mediate the attenuation of AQP4 deficiency to morphine tolerance and dependence. (C)
2008 Elsevier Ireland Ltd. All rights reserved.”
“Reactive PND-1186 cell line oxygen species are thought AZD0530 supplier to be critical inducers of renal inflammation and destruction. We examined the effects of candesartan, a highly selective angiotensin II type I receptor (AT1R) blocker, on renal inflammation and oxidative stress. Candesartan suppressed TNF-induced chemokine expression and NF kappa B activation independent of AT1R blockade in cultured renal tubular epithelial cells. This receptor blocker decreased reactive oxygen generation elicited by either TNF or the pro-oxidant hydrogen
peroxide and reinstated redox homeostasis, suggesting a direct antioxidant effect. This result was unique to candesartan among several angiotensin II receptor blockers and occurred in cells lacking the AT1R. A dose 5 times the standard therapeutic dose lessened renal inflammation and suppressed tubular NF kappa B activation in spontaneously hypertensive rats. An ultrahigh dose ( 15 times standard) produced an even greater beneficial effect. Angiotensin II infusion did not cause any hemodynamic changes at either candesartan dose denoting a complete blockade of systemic and renal AT1R. There was, however, a dose-dependent improvement of renal medroxyprogesterone redox homeostasis. Our study suggests that candesartan suppresses redox-sensitive NF kappa B-mediated renal inflammation by a direct antioxidant effect independent of AT1R blockade.”
“We investigated N400 anomalies and their relationship with neuropsychological disturbance of schizophrenia. Twelve patients with schizophrenia and 12 normal controls, matched for age, sex, education and handedness underwent both the neuropsychological test and the electrophysiological recordings employing semantic violation sentence paradigm. The patients with schizophrenia showed a reduced N400 amplitude and worse performance in the frontal lobe function test compared to healthy participants.