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)

Although research is beginning to clarify the relationship between structure and functional activity in the adult cerebral cortex, little is known about cortical development in the somatosensory cortex of cats. A number of parameters were used in this study to identify functional and anatomical correlates in the developing somatosensory cortex of kittens ranging in age from 3 to 33 d: 2-deoxyglucose (2DG) uptake, cytochrome oxidase (CO) activity, Nissl staining, and AChE activity. All of these parameters were found to reflect an immaturity that evolved to the adult-like pattern by 4-5 weeks of age. Nissl staining revealed an immature laminar pattern at birth, in which layers I, V, and VI were distinct whereas layers II-IV were homogeneous in appearance. Numerous cells could be observed at the layer VI-white matter junction and throughout the white matter, a feature not found in adults. The laminar distribution of Nissl-stained cells gradually became mature by 4-5 weeks of age. CO staining was homogeneous throughout all layers, in contrast to the adult pattern, which displays laminar differentiation. In young animals, many darkly stained CO+ cells were found at the layer VI-white matter border and in the white matter, a distribution not found in the adult. AChE staining in kittens was also distinctly different from that in adults. At birth, AChE+ fibers could be found in layers I, V, and VI but were scarce in layers II-IV. In the adult, a dense network of AChE+ fibers can be found in all layers. 2DG uptake was also immature, as little stimulus-evoked activity could be observed in animals younger than 2 weeks. A dense band of metabolic activity was found in the zone between layer VI and the white matter, whether or not a somatic stimulus was delivered. These results suggest a close correlation between the developing cytoarchitecture and the emergence of a mature pattern of functional activity in the somatosensory cortex.
Cereb Cortex
PMID:Development of cat somatosensory cortex: structural and metabolic considerations. 132 52

The maturation of brain oxidative capacity was studied in kittens, using cytochrome oxidase histochemistry, at different ages throughout development. Optical densitometry values of reacted tissue were obtained for 50 different structures of the brain. In general, most structures reached adult levels of oxidative capacity by 30 days of age with some motor areas (e.g., cerebellum, red nucleus) exhibiting adult values as early as 7 days of age. Thereafter, some structures (e.g., basal ganglia, thalamus) exhibited levels of cytochrome oxidase activity that exceeded adult values for varying periods of time. These findings indicate regional heterogeneity in the maturation of cerebral oxidative capacity. Furthermore, these maturational patterns appear to correlate well with previous observations from anatomical, physiological and neurobehavioral studies.
J Cereb Blood Flow Metab 1992 Nov
PMID:Maturation of cerebral oxidative metabolism in the cat: a cytochrome oxidase histochemistry study. 132 63

The number of GABA-immunoreactive [GABA(+)] neurons and synapses was determined in functionally distinct subregions delineated as rich and poor in cytochrome oxidase (CO) in the visual cortex of adult macaque monkeys. The average numerical density (number per unit volume, Nv) of GABA(+) neurons and synapses was not significantly different between the CO-rich and -poor regions. Twenty percent of the total number of cortical neurons and 17% of the synapses were GABA(+). On average, each visual cortical neuron receives 3900 synapses, 660 of them being GABA(+). The latter were distributed on the target cell in a pattern that predicts the site of GABA influences in cortex. The major targets of GABA(+) synapses were dendritic shafts, comprising nearly two-thirds of the postsynaptic elements. About every fourth and every eighth GABA(+) synapse was devoted to dendritic spines and to neuronal somata, respectively. Axon initial segments, although the exclusive targets of GABA(+) cells, comprise less than 0.1% of structures postsynaptic to GABA(+) boutons. From this distribution, we estimate that in each cubic millimeter of striate cortex there were about 20 million GABA(+) synapses on dendritic spines, 47 million on dendritic trunks, 9 million on somata, and fewer than 0.1 million on axon initial segments. The sites of influences of GABA-immunonegative [GABA(-)] synapses were different in that they target mainly dendritic spines and dendritic trunks. About two-thirds of GABA(-) synapses were on dendritic spines, and the remainder were devoted to dendritic trunks. Only a minute fraction innervate somata. We estimate that in 1 mm3 of striate cortex there were about 235 million GABA(-) synapses on spines, 133 million on dendrites, and about 2 million on somata. The proportions of GABA(+) neurons and synapses and their target distribution did not appreciably differ from those of the visual cortex of the cat even though the numerical density of neurons was 2.5 times higher in the monkey.
Cereb Cortex
PMID:Quantitative distribution of GABA-immunopositive and -immunonegative neurons and synapses in the monkey striate cortex (area 17). 133 Jan 21

Layer IVA of rhesus monkey striate cortex contains pyramidal cells arranged in distinct groups. Their cell bodies are in a configuration of flat cones, each with an average diameter of 60 microns, and their apical dendrites aggregate into bundles that ascend toward the pial surface. Nissl-stained sections suggest that these pyramidal cell cones have their bases in layer IVB, with their tops extending into layer IVA. The neurons in the cones are readily apparent in MAP2 antibody-stained material, and in cytochrome oxidase-reacted tissue it is evident that the pyramidal cell cones occupy the pale spaces that are surrounded by the darkly reactive honeycomb lattice. This lattice of neuropil around the cones contains some axons and boutons that are immunoreactive for parvalbumin, and it is within the lattice that other investigators have shown afferents from the parvocellular (P)-layers of the dLGN to terminate. Because of this input, it is likely that the pyramidal cell cones of layer IVA are involved with color and form perception. The relationship between the layer IVA cones of neurons and the underlying system of previously described pyramidal cell modules (Peters and Sethares, 1991) is discussed, as well as the possibility that the pyramidal cell cones might represent aggregations of neurons, which receive input from basic sets of P-like afferents originating from color-responsive ganglion cells of the retina, as described by Schein and de Monasterio (1987).
Cereb Cortex
PMID:Layer IVA of rhesus monkey primary visual cortex. 172 7

Focal cortical CBF and oxygenation were measured in rats during repetitive seizures to determine whether CBF is maintained above a critical level for adequate delivery of O2. Cerebral oxygenation was determined by measuring relative changes in the oxidation/reduction level of cytochrome aa3 and CBF was measured by the washout of H2. During early seizures, cortical CBF increased to 350% of control and cortical oxygenation also rose markedly. During later seizures, both the increases in CBF and in cortical oxygenation were attenuated progressively. This was accompanied also by attenuation of the associated increases in MABP. Cortical oxygenation decreased during a seizure if the increase in CBF failed to exceed 150-200% of control, defining the critical CBF value. Ventilating the rats on 97% O2 resulted in restoration of the seizure-associated increases in cortical oxygenation in 50% of the cases. The elevation of inspired O2 was effective only if CBF increased once again above 150-200% of control, confirming that the critical CBF lies within this range of values. We conclude that CBF must rise greater than 200% of control levels to provide sufficient O2 to meet the enhanced metabolic requirements of repetitive seizures.
J Cereb Blood Flow Metab 1991 Jan
PMID:Relative hypoperfusion in rat cerebral cortex during recurrent seizures. 184 66

We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of onset of mitochondrial dysfunction and neurologic signs was unclear, in the present study we killed postanoxic cats immediately when signs first appeared. Cerebrocortical homogenates and isolated brain mitochondria only from symptomatic cats showed markedly inhibited substrate-, ADP-, and uncoupler-stimulated respiration rates. Cytochrome oxidase activity and cytochrome aa3 concentrations were also markedly reduced in these mitochondria. Since brain mitochondrial function was impaired when neurologic signs first appeared, mitochondrial alterations are an important early organellar change correlated with development of neurologic deterioration following anoxia.
J Cereb Blood Flow Metab 1990 May
PMID:Delayed onset of neurologic deterioration following anoxia/ischemia coincides with appearance of impaired brain mitochondrial respiration and decreased cytochrome oxidase activity. 215

To examine the relationships between brain glycolysis, ion transport, and mitochondrial reduction/oxidation (redox) activity, extracellular potassium ion activity (K+0) and redox shifts of cytochrome oxidase (cytochrome a,a3) were recorded previous to and during superfusion of rat cerebral cortex with the glycolytic inhibitor iodoacetic acid (IAA). IAA produced oxidation of cytochrome a,a3, increased local oxygenation, increased K+0, and, in response to neuronal activation, slowed rates of K+0 reaccumulation. Rates of rereduction of cytochrome a,a3, after the oxidation of this cytochrome by stimulation, were also slowed by IAA. These effects of IAA demonstrate the dependence of K+0 reaccumulation on the integrity of glycolysis, support the concept that active processes are involved in brain ion transport, and suggest a link between ATP supplied by glycolysis and ion transport activity. These data are also compatible with the suggestion that residual dysfunctions after brain ischemia result from derangements in glycolytic functioning rather than from limitations in oxygen availability or oxidative metabolic activity.
J Cereb Blood Flow Metab 1988 Dec
PMID:Inhibition of glycolysis alters potassium ion transport and mitochondrial redox activity in rat brain. 284 47

This study documents the effects of an intracarotid artery injection of a lethal threshold amount of KCN (2.5 mg.kg-1) on the energy metabolism and histology of the rat brain. This dose of KCN resulted in a rapid abolition of electroencephalographic activity, which remained essentially absent for up to 3 h. Cerebral metabolite measurements 0.25 h after KCN infusion indicated a 52% reduction in cytochrome oxidase activity, a 600% increase in lactate, a 32% reduction in ATP, a 73% increase in ADP, and an 85% decrease in glycogen. Measurements of the above energy metabolites over the ensuing 7 days showed a return to control of all metabolites by 6-24 h. Corresponding to the normalization of energy metabolism was a return of EEG and conscious activity. Histological examination of cyanide-exposed animals revealed a paucity of change with only one animal at 0.5 h showing several dark neurons, two animals at 1 h with minor pallor of corpus callosum and caudate-putamen, and one animal at 48 h with a small hippocampal infarction. It is concluded that it may be impossible to produce a serious enough disruption of cerebral metabolism with KCN injection, to produce neuronal damage by purely "histotoxic" mechanisms.
J Cereb Blood Flow Metab 1989 Apr
PMID:Cerebral energy metabolism in cyanide encephalopathy. 292 Dec 90

Studies in experimental animals and post-mortem studies in humans have indicated that the level of the mitochondrial enzyme cytochrome oxidase within brain anatomical pathways is regulated by the long-term functional use of those pathways. To study this relationship, we have measured cytochrome oxidase spectrophotometrically in punch biopsies from different brain regions of rat. We compared these assays against results from the diaminobenzidine histochemical technique. We found a high degree of correlation (r = 0.90) between the density of diaminobenzidine reaction product and enzyme activity. This validates the usefulness of the diaminobenzidine technique for anatomical localization and measurement of this enzyme. To study the feasibility of using radioactive cyanide as an in vivo ligand of cytochrome oxidase, we performed quantitative autoradiographic analysis of rat brains of animals given an intravenous bolus injection of [14C]cyanide. Analysis of the arterial blood curve indicated a complex redistribution of cyanide between red blood cells, plasma, and tissues. Brain labeling reached peak levels at 1 min and then fell despite rising concentrations of free plasma cyanide. Analysis of autoradiographic images revealed good anatomical resolution. The density of labeling in individual structures over time failed to show a strong correlation with cytochrome oxidase activity or diaminobenzidine reaction product.
J Cereb Blood Flow Metab 1986 Feb
PMID:Distribution of cytochrome oxidase in rat brain: studies with diaminobenzidine histochemistry in vitro and [14C]cyanide tissue labeling in vivo. 300 31

This study was directed at relating ion transport and mitochondrial redox activity during hypoxia, as a step toward definition of brain oxygen sufficiency. To accomplish this, extracellular potassium ion activity (K+o) was recorded by ion-selective microelectrodes while reduction/oxidation (redox) ratios of cytochrome oxidase (cytochrome a,a3) were monitored by reflection spectrophotometry in cerebral cortex of rats anesthetized with pentobarbital. In normoxia, neuronal activation by direct cortical stimulation produced transient oxidation of cytochrome a,a3 and elevation of K+o. Moderate hypoxia (PaO2 above 50 mm Hg) resulted in reduction of cytochrome a,a3 but only slight elevation of K+o. At this level of hypoxia, cytochrome a,a3 continued to respond to neuronal activation with transient shifts toward oxidation and rates of K+o reaccumulation were unchanged from control. When PaO2 was further decreased below a critical threshold, stimulus-provoked oxidative responses of mitochondrial reactants were replaced by shifts toward reduction, but rates of reaccumulation of K+, spilled into the extracellular space by neuronal activation, remained unchanged. Only during severe hypoxia (PaO2 less than 20 mm Hg) was it possible in some animals to record a slowing in the reaccumulation of K+o without provocation of spreading cortical depression. These data indicate that ion transport activity in cerebral cortex is more refractory to hypoxia than is mitochondrial redox functioning. They suggest an in vivo parallel to the "cushioning" effect of mitochondria in vitro, in which oxygen consumption remains constant despite fluctuations in oxygenation and redox ratios, and also that there may be a greater anaerobic capacity to provide energy for ion transport in mammalian brain than has previously been appreciated.
J Cereb Blood Flow Metab 1988 Apr
PMID:Potassium ion homeostasis and mitochondrial redox activity in brain: relative changes as indicators of hypoxia. 334 90


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