Microinjection of monosodium glutamate into the IVN also inhibited the JOR ipsilaterally. These results suggest that the VN is involved in modulation of the JOR and plays an important role in controlling the jaw movements. (C) 2009 Elsevier

Ireland Ltd. All rights reserved.”
“The herpes simplex virus type 1 (HSV-1) gene UL12 encodes a conserved alkaline DNase with orthologues in all herpesviruses. The HSV-1 UL12 gene gives rise to two separately promoted 3′ coterminal mRNAs which encode distinct but related proteins: full-length UL12 and UL12.5, an amino-terminally truncated form that initiates at UL12 codon 127. Full-length UL12 localizes to the nucleus where it promotes the generation of mature viral genomes from larger precursors. CA-4948 datasheet In contrast, UL12.5 is predominantly AZD1390 manufacturer mitochondrial and acts to trigger degradation of the mitochondrial genome early during infection. We examined the

basis for these very different subcellular localization patterns. We confirmed an earlier report that the amino-terminal region of full-length UL12 is required for nuclear localization and provide evidence that multiple nuclear localization determinants are present in this region. In addition, we demonstrate that mitochondrial localization of UL12.5 relies largely on sequences located between UL12 residues 185 and 245 (UL12.5 residues 59 to 119). This region contains a sequence that resembles a typical mitochondrial matrix localization signal, and mutations that reduce the positive charge of this element severely impaired mitochondrial localization. Consistent with matrix localization, UL12.5 displayed a detergent extraction profile indistinguishable from that of the matrix protein cyclophilin D. Mitochondrial DNA depletion required the exonuclease Protein kinase N1 activity of UL12.5, consistent

with the idea that UL12.5 located within the matrix acts directly to destroy the mitochondrial genome. These results clarify how two highly related viral proteins are targeted to different subcellular locations with distinct functional consequences.”
“Intestinal electrical stimulation (IES) has been shown to produce inhibitory effects on gastric contractions, gastric emptying, food intake and body weight in rats and dogs, suggesting a therapeutic potential for obesity. The aims of this study were (1) to test the hypothesis that the neurons in the VMH are involved in the central mechanisms of IES treatment for obesity; (2) to compare the effects of IES at the duodenum and IES at the ileum on neuronal activities of the VMH; (3) to better understand if the neuronal activity modulated by IES was mediated via the vagal pathway. Extracellular potentials of neurons in the VMH were recorded in 18 anesthetized rats.