We examined RNF11 expression levels

in correlation to phospho-p65, a marker for activated NF-kappa B, in control and PD brain tissue from cerebral cortex. In addition we performed double immunofluorescence labeling experiments to confirm this correlation. Our investigations demonstrated that the neuronal RNF11 expression was down-regulated in PD and was usually associated with increased expression of phospho-p65. Double labeling confirmed that loss of neuronal RNF11 was linked to increased phospho-p65 expression, suggesting that persistent presence of NF-kappa B activation could be due to decreased levels of its negative regulator. Our data exemplifies the relevance of RNF11 and persistent NF-kappa B activation in PD. (c) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Epidermal growth factor (EGF) and its family member neuregulin-1 are implicated in the etiology of schizophrenia. EPZ5676 ic50 Our recent pharmacological studies indicate that EGF injections to neonatal see more and adult rats both induce neurobehavioral deficits relevant to schizophrenia. We, however, did not evaluate the genetic impact of EGF transgene on neurobehavioral traits. Here we analyzed transgenic mice carrying the transgene of mouse

EGF cDNA. As compared to control littermates, heterozygous EGF transgenic mice had an increase in EGF mRNA levels and showed significant decreases in prepulse inhibition and context-dependent fear learning, but there were no changes in locomotor behaviors and sound startle responses. In addition, these transgenic mice exhibited higher behavioral sensitivity to the repeated cocaine injections. There were neurochemical alterations in metabolic enzymes of dopamine (i.e., tyrosine hydroxylase, dopa decarboxylase, catechol-O-methyl transferase) and monoamine contents in various brain regions of the EGF transgenic mice, but there were no apparent neuropathological signs in the brain. The present findings rule out the indirect influence of anti-EGF antibody production on the reported behavioral deficits of EGF-injected

mice. These results support the argument that aberrant hyper-signals of EGF have significant Pevonedistat impact on mouse behavioral traits and dopamine metabolism. (c) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Background and aim: Curcumin at 100 mg/kg has been shown to have a protective effect on crush nerve injury. However, it is unclear whether the protective effect of curcumin on nerve injury is dose dependent. The present study was designed to investigate such a possibility. Methods: The rats subjected to crush nerve injury were intraperitoneally administrated daily for 4 weeks with curcumin (50 mg/kg, 100 mg/kg and 300 mg/kg), or 100 mu g/kg mecobalamin or normal saline, respectively. The axonal regeneration was investigated by retrograde labeling and morphometric analysis. The motor functional recovery was evaluated by electrophysiological studies, behavioral tests and histological appearance of the target muscles.