Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lipid composition of highly purified Flury strain of rabies virus (HEP) propagated in BHK-21 cells in a chemically defined medium was observed to be 6.7% neutral lipids, 15.8% phospholipids, and 1.5% glycolipids. In the virion, phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin were the most abundant phospholipids, accounting for 90% of the total, and the molar ratio of cholesterol to phospholipid was 0.48. Uninfected BHK-21 cell membranes were obtained by nitrogen cavitation techniques and separated by density gradient centrifugation, and the membranes were assayed for purity using 5'-nucleotidase, cytochrome oxidase, and reduced nicotinamide adenine dinucleotide phosphate diaphorase activities. Lipids of the plasma membrane were enriched in cholesterol, phosphatidylcholine, and phosphatidylethanolamine. In contrast, membranes of the endoplasmic reticulum were enriched in phosphatidylcholine, but contained smaller amounts of phosphatidylethanolamine and sphingomyelin. Comparison of the fatty acyl chains of virus and membranes from uninfected cells revealed the virion to have the lowest ratio of C18:1 to C18:0 (1.771), compared with values of about 3.0 for the plasma membrane and endoplasmic reticulum. Total polyenoic fatty acids were enriched in the plasma membrane, whereas the virus contained higher amounts of total saturates than either of the two membrane preparations. Analysis of the polar and neutral lipid fractions as well as the acyl chain analysis suggests the virion has a lipid composition that is intermiediate to that of the plasma membrane and endoplasmic reticulum and is consistent with the view that numerous viral particles are synthesized de novo by not utilizing a preexisting membrane template. From the ratio of cholesterol to phospholipid of 0.48, we calculated that 1.92 X 10(5) molecules of lipid would cover 4.14 X 10(4) nm2 in the form of a bilayer. Considerations of the molecular dimensions of the rabies envelope (total surface area, 5 X 10(4) nm2) as a bilayer suggest that some penetration of lipids by envelope proteins (M and G) is necessary.
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PMID:Lipids of rabies virus and BHK-21 cell membranes. 55 73

Parallel pathways in the primate visual system parse the sensory signal into magnocellular (M), parvocellular (P), and koniocellular (K) streams. These pathways remain anatomically separate and distinct from their origination in different retinal ganglion cell types, through distinct layers of the lateral geniculate nucleus, and into primary visual cortex (V1), with the M pathway terminating primarily in layer 4Calpha, the P pathway in layer 4Cbeta, and the K pathway in the cytochrome oxidase blobs of layer 2/3. Recent studies indicate that outputs from V1 are less compartmental than previously thought, making it difficult to assess the contributions of M and P pathways to areas beyond V1 in the dorsal and ventral streams. Here we use rabies virus as a retrograde transsynaptic tracer to study the contributions of M and P pathways to areas middle temporal (MT), V3, and V2 of macaque monkey. We find that, although disynaptic inputs through layer 4C of V1 to dorsal stream area MT are dominated by the M pathway, within an additional three synapses MT receives a substantial P input. This P input is unlikely to reach MT via V3, which we show also receives disynaptic inputs dominated by the M pathway. We find that disynaptic inputs to V2, however, can be more balanced and may carry convergent M and P input to MT. Our observations provide evidence for multiple pathways from V1 to MT, with varying degrees of M and P convergence. Each pathway likely provides functionally specialized information to MT and dorsal stream visual processing.
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PMID:Multiple circuits relaying primate parallel visual pathways to the middle temporal area. 1715 Dec 82

Primary visual cortex recombines inputs from magnocellular (M) and parvocellular (P) streams to create functionally specialized outputs. Understanding these input-output relationships is complicated by the fact that layer 4B, which provides outputs to dorsal visual areas, contains multiple cell types. Using a modified rabies virus that expresses green fluorescent protein, we show that layer 4B neurons projecting to MT are a majority spiny stellate, whereas those projecting to V2 are overwhelmingly pyramidal. Regardless of cell type, MT-projecting neurons have larger cell bodies, more dendritic length, and are deeper within layer 4B. Furthermore, MT-projecting pyramidal neurons are located preferentially underneath cytochrome oxidase blobs, indicating that MT-projecting neurons of both types restrict their dendrites to M-recipient zones. We conclude that MT-projecting layer 4B neurons are specialized for the fast transmission of information from the M pathway, while V2-projecting neurons are likely to mediate slower computations involving mixed M and P signals.
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PMID:Specialized circuits from primary visual cortex to V2 and area MT. 1778 86

Parallel visual pathways in the primate brain known as the dorsal and ventral streams receive retinal inputs mainly through the magnocellular (M) and parvocellular (P) layers of the lateral geniculate nucleus. Inputs from these layers terminate within distinct parts of layer 4C of V1 (visual area 1). Due to the complexity of M- and P-derived neural connectivity in V1 and higher visual areas, the contributions of M and P inputs to the dorsal and ventral streams remain unclear. Employing retrograde transsynaptic transport of rabies virus, we analyzed the architecture of bottom-up pathways toward ventral stream area V4 (visual area 4) and dorsal stream area MT (middle temporal area). We found that V4 receives both M and P inputs "trisynaptically" from layer 4C via layer 2/3 of V1, whereas MT receives M-dominant input "disynaptically" from layer 4C via layer 4B of V1. V4 also receives disynaptic input from the dorsal stream portion of V2 (visual area 2) (i.e., cytochrome oxidase-stained thick stripes). Moreover, both M and P inputs reach V4 trisynaptically and MT disynaptically through "short-cut" pathways that bypass layer 4C of V1. The differential patterns of multisynaptic geniculo-cortical pathways to V4 and MT imply distinct modes of information processing in the dorsal and ventral streams.
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PMID:Differential architecture of multisynaptic geniculo-cortical pathways to V4 and MT. 2151 14

Infection with the challenge virus standard-11 (CVS) strain of fixed rabies virus induces neuronal process degeneration in adult mice after hindlimb footpad inoculation. CVS-induced axonal swellings of primary rodent dorsal root ganglion neurons are associated with 4-hydroxy-2-nonenal protein adduct staining, indicating a critical role of oxidative stress. Mitochondrial dysfunction is the major cause of oxidative stress. We hypothesized that CVS infection induces mitochondrial dysfunction leading to oxidative stress. We investigated the effects of CVS infection on several mitochondrial parameters in different cell types. CVS infection significantly increased maximal uncoupled respiration and complex IV respiration and complex I and complex IV activities, but did not affect complex II-III or citrate synthase activities. Increases in complex I activity, but not complex IV activity, correlated with susceptibility of the cells to CVS infection. CVS infection maintained coupled respiration and rate of proton leak, indicating a tight mitochondrial coupling. Possibly as a result of enhanced complex activity and efficient coupling, a high mitochondrial membrane potential was generated. CVS infection reduced the intracellular ATP level and altered the cellular redox state as indicated by a high NADH/NAD+ ratio. The basal production of reactive oxygen species (ROS) was not affected in CVS-infected neurons. However, a higher rate of ROS generation occurred in CVS-infected neurons in the presence of mitochondrial substrates and inhibitors. We conclude that CVS infection induces mitochondrial dysfunction leading to ROS overgeneration and oxidative stress.
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PMID:Mitochondrial dysfunction in rabies virus infection of neurons. 2427 36