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

The pattern of peripheral nerve inputs into the dorsal column nuclei, cuneate and gracile, was investigated in the prosimian Galago garnetti. The major findings were, that there is a greater segregation of the inputs from the fingers/hand within the cuneate compared with input form the toes/foot within the gracile. In both nuclei, cell clusters can be identified as cytochrome oxidase dense blotches, reactive also for the activity-dependent enzyme nitric oxide synthase. In the cuneate, cell clusters were apparent as six main cytochrome oxidase/nitric oxide synthase-reactive ovals arranged in a medial to lateral sequence. In contrast in the gracile, a higher degree of parcellation was noted and several cytochrome oxidase/nitric oxide synthase blotches were distributed along the rostrocaudal axis of the nucleus. This different architecture parallels differences in the organization of the inputs from the hand and from the foot. In the cuneate, cholera toxin B subunit conjugated to horseradish peroxydase labeled terminals from the glabrous and hairy skin of digits d1 to d5 segregated in each of the five most lateral cytochrome oxidase/nitric oxide synthase blotches. Afferents from the thenar, palmar pads and hypothenar overlapped with those from digit 1, digit 2 to digit 4 and digit 5, respectively. Inputs from wrist arm and shoulder were segregated in the most medial blotch. In the gracile, multiple foci of cholera toxin B subunit conjugated to horseradish peroxydase labeled terminals were observed upon injections of single sites in the toes or plantar pads. Although in multiple foci, inputs from different toes segregated from one another as well. Terminals from the plantar pads appeared to converge on the same cytochrome oxidase/nitric oxide synthase blotches targeted by inputs from the toes. In both the cuneate and the gracile, cytochrome oxidase/nitric oxide synthase blotches also presented intense immunoreactivity for GABA, calbindin, parvalbumin, and brain derived neurotrophic factor. Finally, in the cuneate the cell cluster region presented similarities in prosimian galagos and four species of New World monkeys, whereas it appeared more differentiated and complex in the Old Word macaque monkeys. In conclusion, the different pattern of segregation of the inputs from the hand and from the foot can be related to the different metabolic organization of the cuneate and of the gracile, respectively.
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PMID:The chemo- and somatotopic architecture of the Galago cuneate and gracile nuclei. 1257 23

Studies have suggested that ketamine, a nonselective NMDA receptor antagonist, could be a new drug in the treatment of major depression, but the way ketamine presents such effects remains to be elucidated. Therefore, the objective of this paper was to evaluate the effects of ketamine treatment on parameters related to depression in the brain of adult rats subjected to an animal model of depression. The animals were divided into: non-deprived + saline; non-deprived + ketamine; deprived + saline; deprived + ketamine. Treatments involving ketamine (15 mg/kg) were administered once a day during 14 days in the animal's adult phase. After treatment, the brain derived-neurotrophic factor (BDNF) levels, oxidative stress and energy metabolism activity were evaluated in brain structures of rats involved in the circuit of depression. In the amygdala, hippocampus and nucleus accumbens (NAc), a reduction in BDNF levels was observed in deprived rats, but the animals treated with ketamine reversed the effects of this animal model only in the amygdala and NAc. In addition to this, the complex I activity, in deprived rats, was diminished in the prefrontal cortex (PFC) and amygdala; in the PFC and hippocampus, the complex II-III was diminished in deprived rats; still the administration of ketamine increased the complex IV activity in the PFC and amygdala of rats submitted to the maternal deprivation. In deprived rats, the creatine kinase activity was reduced in the PFC and amygdala, however the administration of ketamine reversed this decrease in the amygdala. The malondialdehyde (MDA) equivalents were increased in non-deprived rats treated with ketamine in the PFC and NAc. Carbonyl levels in the PFC were diminished in control rats that received saline. Though ketamine treatment reversed this effect in deprived rats in the PFC and hippocampus. Still, in NAc, the carbonyl levels were diminished in deprived rats. The superoxide dismutase (SOD) activity was increased in control rats that received ketamine in the PFC and NAc, and were diminished in deprived rats that received saline or ketamine in the PFC and hippocampus. These findings may help to explain that dysfunctions involving BDNF, oxidative stress and energy metabolism within specific brain areas, may be linked with the pathophysiology of depression, and antidepressant effects of ketamine can be positive, at least partially due to the control of these pathways.
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PMID:Ketamine treatment partly reverses alterations in brain derived- neurotrophic factor, oxidative stress and energy metabolism parameters induced by an animal model of depression. 2561 82

Mitochondrial protein (MP) assemblies undergo alterations during neurogenesis, a complex process vital in brain homeostasis and disease. Yet which MP assemblies remodel during differentiation remains unclear. Here, using mass spectrometry-based co-fractionation profiles and phosphoproteomics, we generated mitochondrial interaction maps of human pluripotent embryonal carcinoma stem cells and differentiated neuronal-like cells, which presented as two discrete cell populations by single-cell RNA sequencing. The resulting networks, encompassing 6,442 high-quality associations among 600 MPs, revealed widespread changes in mitochondrial interactions and site-specific phosphorylation during neuronal differentiation. By leveraging the networks, we show the orphan C20orf24 as a respirasome assembly factor whose disruption markedly reduces respiratory chain activity in patients deficient in complex IV. We also find that a heme-containing neurotrophic factor, neuron-derived neurotrophic factor [NENF], couples with Parkinson disease-related proteins to promote neurotrophic activity. Our results provide insights into the dynamic reorganization of mitochondrial networks during neuronal differentiation and highlights mechanisms for MPs in respirasome, neuronal function, and mitochondrial diseases.
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PMID:Rewiring of the Human Mitochondrial Interactome during Neuronal Reprogramming Reveals Regulators of the Respirasome and Neurogenesis. 3153 60