Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 neuronal uptake and laminar distribution of cortically injected tritium-labeled gamma-aminobutyrate (GABA), aspartic acid, glutamate and glycine was examined in the prestriate cortex of squirrel monkeys. The intent of this investigation was not to examine the role of these amino acids as neurotransmitters, but to correlate the distribution of tritium-labeled neurons with their levels of cytochrome oxidase activity. A comparison of the number of these labeled neurons was made between the metabolically active "puff" and the less active "nonpuff" regions. In addition, these results were contrasted with the findings in area 17. With each tritiated amino acid tested, labeled neurons that had either high or low levels of cytochrome oxidase activity were present in all laminae. However, the density of labeled neurons varied between lamina for a given amino acid as well as between different amino acids. While many neurons that were cytochrome oxidase-reactive were also tritium-labeled, cytochrome oxidase activity was not a prerequisite for the sequestering of tritium label. In fact, many of the labeled neurons exhibited relatively low levels of cytochrome oxidase activity. Similar to area 17, few aspartate- or glutamate-labeled neurons were present in laminae II-III. The number of labeled neurons for both amino acids increased in laminae IV-VI, with the greatest increase observed in laminae V-VI. Gamma-aminobutyrate-labeled neurons were more prevalent in laminae I and upper II than in the other laminae, whereas in area 17, a greater proportion of the labeled neurons were found in laminae V-VI. With the exception of the uppermost laminae, where GABA-labeled neurons were more abundant, the number of glycine-labeled neurons was significantly greater throughout most laminae than with the other amino acids examined. The density of glycine-labeled neurons in lamina IV, however, was significantly less than the number observed in lamina III even though lamina III was farther away from the injection site which was at the boundary between laminae V-VI. Glycine-labeled neurons were, on average, larger than those labeled with any other amino acid. Similar to area 17, more GABA- and glycine-labeled neurons were observed within the puff regions than in nonpuff regions. No puff/nonpuff differences were observed in the distribution of leucine-injected controls. Labeled neurons for each amino acid included stellate-, fusiform- and pyramidal-shaped cells, each of varying sizes. However, outside the intensely labeled injection sites, no GABA-labeled pyramidal cells were observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuronal uptake and laminar distribution of tritiated aspartate, glutamate, gamma-aminobutyrate and glycine in the prestriate cortex of squirrel monkeys: correlation with levels of cytochrome oxidase activity and their uptake in area 17. 289 Jan 20

Degeneration of the thalamic fibers in the visual cortex of turtles leads to an increase in the numerical density of cortical synapses with flattened vesicles and symmetrical membrane differentiations (Smith, L. M., and F. F. Ebner (1980) Soc. Neurosci. Abstr. 6: 328). This change correlates with an increase in the cortical activity of glutamic acid decarboxylase (GAD), the synthetic enzyme for gamma-aminobutyric acid (GABA). These data are consistent with the hypothesis that removal of thalamic input activity is the stimulus for cortical GABAergic neurons to form new synapses. Pharmacological evidence suggests that even simple environmental deprivation may induce a similar increase in the numerical density of GABAergic synapses in kitten striate cortex (Duffy, F. H., S. R., Snodgrass, J. L. Burchfiel, and J. L. Conway (1976) Nature 260: 256-257). We have examined this possibility in monocularly deprived kittens using methods to localize and measure GAD. GAD in kitten striate cortex was localized using immunocytochemistry. GAD-positive cells were found in all layers and were uniformly distributed in layers II to VI. Immunoreactivity associated with axon terminals (puncta), in contrast, was laminated with a distinct band in layer IV. Monocular deprivation (MD), by either unilateral enucleation or lid closure, had no detectable effect on the distribution of GAD in striate cortex. The band of layer IV puncta remained uniform even under conditions that produced alterations in layer IV cytochrome oxidase activity. We measured GAD activity in homogenates of striate cortex to address the possibility that MD causes an absolute change in the density of GABAergic synapses. Again, however, GAD activity in the binocular and monocular segments of striate cortex was found to be unaffected by early enucleation. These data suggest two conclusions: first, that the numerical density of GABAergic synapses in visual cortex is not regulated directly by thalamic activity, and second, that changes in GABAergic synapse density do not account for the ocular dominance shift observed in kitten striate cortex after MD.
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PMID:Glutamic acid decarboxylase in the striate cortex of normal and monocularly deprived kittens. 298 36

Antisera to glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid (GABA) have been used to characterize the morphology and distribution of presumed GABAergic neurons and axon terminals within the macaque striate cortex. Despite some differences in the relative sensitivity of these antisera for detecting cell bodies and terminals, the overall patterns of labeling appear quite similar. GABAergic axon terminals are particularly prominent in zones known to receive the bulk of the projections from the lateral geniculate nucleus; laminae 4C, 4A, and the cytochrome-rich patches of lamina 3. In lamina 4A, GABAergic terminals are distributed in a honeycomb pattern which appears to match closely the spatial pattern of geniculate terminations in this region. Quantitative analysis of axon terminals that contain flat vesicles and form symmetric synaptic contacts (FS terminals) in lamina 4C beta and in lamina 5 suggest that the prominence of GAD and GABA axon terminal labeling in the geniculate recipient zones is due, at least in part, to the presence of larger GABAergic axon terminals in these regions. GABAergic cell bodies and their initial dendritic segments display morphological features characteristic of nonpyramidal neurons and are found in all layers of striate cortex. The density of GAD and GABA immunoreactive neurons is greatest in laminae 2-3A, 4A, and 4C beta. The distribution of GABAergic neurons within lamina 3 does not appear to be correlated with the patchy distribution of cytochrome oxidase in this region; i.e., there is no significant difference in the density of GAD and GABA immunoreactive neurons in cytochrome-rich and cytochrome-poor regions of lamina 3. Counts of labeled and unlabeled neurons indicate that GABA immunoreactive neurons make up at least 15% of the neurons in striate cortex. Layer 1 is distinct from the other cortical layers by virtue of its high percentage (77-81%) of GABAergic neurons. Among the other layers, the proportion of GABAergic neurons varies from roughly 20% in laminae 2-3A to 12% in laminae 5 and 6. Finally, there are conspicuous laminar differences in the size and dendritic arrangement of GAD and GABA immunoreactive neurons. Lamina 4C alpha and lamina 6 are distinguished from the other layers by the presence of populations of large GABAergic neurons, some of which have horizontally spreading dendritic processes. GABAergic neurons within the superficial layers are significantly smaller and the majority appear to have vertically oriented dendritic processes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Distribution of GABAergic neurons and axon terminals in the macaque striate cortex. 368 Jun 25

Striking correlations between structure and function are found in the visual cortex of Old World primates. These include the co-localization of glutamic acid decarboxylase (GAD, the biosynthetic enzyme of the inhibitory neurotransmitter, gamma-aminobutyric acid) with the mitochondrial enzyme, cytochrome oxidase (CO) in functionally distinct subcompartments of ocular dominance columns. We report here immunocytochemical studies with a monoclonal antibody (CAT 301) showing that the antibody recognizes an uncharacterized antigen on surfaces of some neurones in certain layers of the monkey striate cortex (area 17), and in certain parts of the cat and monkey dorsal lateral geniculate nuclei (LGN). Patches of immunocytochemically stained neurones and neuropil, apparent in layers III, IVB and VI of the striate cortex of normal monkeys, become even more clearly delineated in animals from which one eye has been removed. The antibody-stained patches in the three layers line up radially with one another in lines passing through the centres of ocular dominance columns (demonstrable by CO staining in layers IVA and IVC). In layers III and VI the patches coexist with CO-positive patches and, in the horizontal dimension, both antibody and CO-positive patches are aligned to form rows. Stained neurones in the monkey LGN are primarily in the magnocellular layers and in the cat LGN are confined to laminae A and A1, the inter-laminar plexuses, the perigeniculate nucleus and the medial inter-laminar nucleus. The antigen we have localized is associated with particular cell populations, some of which may correspond to a specific, physiological class.
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PMID:Monoclonal antibody that identifies subsets of neurones in the central visual system of monkey and cat. 669 27

Bush babies possess three distinct parallel pathways to striate cortex (V1 or area 17). The calcium-binding proteins parvalbumin (PV) and calbindin (CB) typically show complementary regional distributions in the brain, often associated with specific aspects of functionally related groups of cells. We asked whether PV+ and CB+ immunoreactivity differentiate central visual parallel pathways in this species. Results show that PV and CB cell and neuropil staining is strongly complementary in the lateral geniculate nucleus (LGN) and is associated with separate parallel pathways. CB+ immunoreactivity is dense, but cytochrome oxidase (CO) staining is light in the paired koniocellular layers. PV+ and CO+ immunoreactivity is most dense in the parvocellular and magnocellular layers. Combined analyses of cell size, retrograde labeling, and double labeling have confirmed that all PV+ and CB+ LGN cells are geniculocortical relay cells; none was found to be gamma-aminobutyric acid (GABA)ergic. In V1, dense PV+ neuropil closely matches the expression of CO in layer 4 and in the blobs of layer 3. CB+ staining is most dense in layers 2 and 3A and is not strongly expressed within the CO interblobs. Finally, PV and CB are not found in related parallel pathway components in the LGN and V1 (e.g., in V1, CO blobs exhibit dense PV+ neuropil, yet they are targets of the small K geniculocortical relay cells that are CB+ in the LGN). Our findings support the view that three functionally distinct visual pathways project to V1 from the LGN. However, the differences in the patterns of localization of PV and CB in the LGN and in V1 suggest that these proteins may be utilized in different ways in these two visual areas.
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PMID:Distribution of calcium-binding proteins within the parallel visual pathways of a primate (Galago crassicaudatus). 762 17

The pathogenesis of brain dysfunction in a canine model of juvenile Batten disease was studied with techniques designed to determine sequential changes in mitochondrial morphology and cytochrome oxidase (CO) activity, and in neurons and synapses using gamma-aminobutyric acid (GABA) as a neurotransmitter. Histochemical and immunocytochemical methods were employed. Mitochondrial alterations were found in a select population of nonpyramidal neurons in neocortex and claustrum, and in cerebellar basket cells. Proportions of affected neurons at any one time remained constant over the disease course, with morphologically-abnormal mitochondria first being recognized at age 6 months. Enlarged mitochondria were readily identifiable at the light microscope (LM) level as large CO-positive or mitochondrial antibody-positive granular structures. Colabelling with antibodies to GABA or to parvalbumin (PV) indicated that most of these cells were GABAergic. Ultrastructurally, atypical mitochondria were characterized by globular enlargement, intramitochondrial membranous inclusions, and disorganized internal structure. CO activity in all other cell somata and in neuropil was diminished compared with normal, age-matched tissue. Glutamic acid decarboxylase (GAD), PV, and GABA studies demonstrated loss of GABAergic neurons and synapses in cortex and cerebellum of affected dogs. These results indicate that abnormal mitochondria are present in neurons in Batten disease, and suggest that suboptimal mitochondrial function may play a role in the pathogenic mechanisms of brain dysfunction in this disorder.
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PMID:Morphological alterations in neocortical and cerebellar GABAergic neurons in a canine model of juvenile Batten disease. 766 31

Sensory and motor pathways in the central nervous system (CNS) of macaque monkeys were visualized by anterograde or retrograde axonal transport of wheatgerm agglutinin-horseradish peroxidase (WGA-HRP) reacted with the chromagen tetramethylbenzidine (TMB), or by the use of anterograde degeneration after specific ablation lesions. To maximize information from each animal we combined the results of the anterograde and retrograde axonal transport with several pre- and post-embedding markers at both the light and electron microscopic levels while maintaining good preservation of tissue. Pre-embedding techniques included those for cytochrome oxidase activity and the calcium-binding proteins calbindin D-28k and parvalbumin. Post-embedding techniques included immunocytochemistry for gamma-aminobutyric acid (GABA) or other amino acid neurotransmitters. We believe that the methods described here provide superior tissue preservation, thus permitting a more detailed analysis of tissue prepared after experiments concerned with neural circuitry.
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PMID:Electron microscopic imaging of multiple markers in glutaraldehyde fixed CNS tissue of Macaca fascicularis: maximizing information from a single experimental animal. 775 80

The purpose of the present study was to examine the effects of retinal impulse blockade on gamma-aminobutyric acid (GABA)-immunoreactive (GABA-IR) neurons in cytochrome oxidase (CO)-rich puffs of the adult monkey striate cortex. Specifically, we wished to know if changes occurred in their CO activity, GABA immunoreactivity, and synaptic organization. A double-labeling technique, which combined CO histochemistry and postembedding GABA immunocytochemistry on the same ultrathin sections, was used to reveal simultaneously the distribution of the two markers. We quantitatively compared changes in GABA-IR neurons of deprived puffs (DPs) with respect to non-deprived puffs (NPs) 2 weeks after monocular tetrodotoxin treatment. We found that the proportion of darkly CO reactive mitochondria in GABA-IR neurons of DPs drastically decreased to about half of those in NPs. There was a greater reduction of CO levels in GABA-IR axon terminals than in their cell bodies and dendrites. In contrast, most non-GABA-IR neurons displayed no significant change in their CO levels. Morphologically, GABA-IR neurons and axon terminals in DPs showed a significant shrinkage in their mean size. GABA immunoreactivity, as indicated by the density of immunogold particles in GABA-IR neurons, declined in DPs, and a greater decrease was also found in axon terminals than in cell bodies or dendrites. Moreover, the numerical density of GABA-IR axon terminals and synapses in DPs was significantly reduced without changes in that of asymmetric and symmetric synapses. Thus, the present results support the following conclusions: 1) Oxidative metabolism and neurotransmitter expression in GABA-IR neurons are tightly regulated by neuronal activity in adult monkey striate cortex; 2) GABA-IR neurons are much more vulnerable to functional deprivation than non-GABA-IR ones, suggesting that these inhibitory neurons have stringent requirement for sustained excitatory input to maintain their heightened oxidative capacity; and 3) intracortical inhibition mediated by GABA transmission following afferent deprivation may be decreased in deprived puffs, because the oxidative capacity and transmitter level in GABAergic neurons, especially in their axon terminals, are dramatically reduced.
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PMID:Metabolic and neurochemical plasticity of gamma-aminobutyric acid-immunoreactive neurons in the adult macaque striate cortex following monocular impulse blockade: quantitative electron microscopic analysis. 879 61

We suggest that a dysregulation of energy metabolism in the brain of genetic absence epilepsy rats from Strasbourg (GAERS) could create a specific cerebral environment that would favor the expression of spike-and-wave discharges (SWD) in the thalamocortical loop, largely dependent on glutamatergic and gamma-aminobutyric acid (GABA)-ergic neurotransmissions. We tested several aspects of metabolic activity in the brain of GAERS compared to a genetic strain of nonepileptic (NE) rats. Glucose metabolism was higher in all brain regions of GAERS compared to those of NE rats along the whole glycolytic and aerobic pathways, as assessed by regional histochemical measurement of lactate dehydrogenase and cytochrome oxidase activities. Branched-chain amino acids (BCAA) and alpha-ketoisocaproate (alpha-KIC), the ketoacid of leucine, when injected intraperitoneally, increased the number of SWD in GAERS but had only a slight effect on their duration. These data speak in favor of a BCAA- or alpha-KIC-induced change in neuronal excitability. Leucine and alpha-KIC decreased the concentration of glutamate in thalamus and cortex without affecting GABA concentrations. Thus, BCAA and alpha-KIC, by decreasing glutamatergic neurotransmission, could favor GABAergic neurotransmission, which is known to increase the occurrence of seizures in GAERS. Finally, the transport of [1-(14)C]alpha-KIC in freshly isolated cortical neurons was lower in GAERS than in NE rats, and this difference was shown to be of metabolic origin. The addition of gabapentin, a specific inhibitor of BCAA transaminase (BCAT), reduced the transport of [1-(14)C]alpha-KIC in GAERS and NE rats to a level that became identical in both strains. This strain-dependent change was not related to a difference in the activity of BCAT, which was identical in GAERS and NE rats. The exact origin of this apparent metabolic dysregulation of energy metabolism in GAERS that could underlie the origin of seizures in that strain remains to be explored further.
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PMID:Metabolic approach of absence seizures in a genetic model of absence epilepsy, the GAERS: study of the leucine-glutamate cycle. 1174 20

As in other primates, the lateral geniculate nucleus (LGN) of owl monkeys contains three anatomically and physiologically distinct relay cell classes, the magnocellular (M), parvocellular (P), and koniocellular (K) cells. M and P LGN cells send axons to the upper and lower tiers of layer IV, and K cells send axons to the cytochrome oxidase (CO) blobs of layer III and to layer I of primary visual cortex (V1). Our objective was to compare the synaptic arrangements made by these axon classes. M, P, and K axons were labeled in adult owl monkeys by means of injections of wheat germ agglutinin-horseradish peroxidase into the appropriate LGN layers. The neurochemical content of both pre- and postsynaptic profiles were identified by postembedding immunocytochemistry for gamma-aminobutyric acid (GABA) and glutamate. Our key finding is that the synaptic arrangements made by M, P, and K axons in owl monkey exhibit more similarities than differences. They are exclusively presynaptic, contain glutamate and form asymmetric synapses mainly with glutamate-positive dendritic spines. The majority of the remaining axons synapse with glutamatergic dendritic shafts. There are also differences between LGN pathways. M and P terminals are significantly larger and more likely to make multiple synapses than K axons, although M and P axons do not differ from each other in either of these characteristics. Of interest, a larger percentage of M and K axons than P axons make synapses with GABAergic dendritic shafts. Cells directly postsynaptic to M and K axons are known to exhibit orientation selectivity and, in some cases, direction selectivity. Cells postsynaptic to P axons do not show these properties, but instead tend to reflect their LGN inputs more faithfully; therefore, it is possible that these physiologic differences seen in the cortical cells postsynaptic to different LGN pathways reflect the differential involvement of inhibitory circuits.
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PMID:Neurochemical comparison of synaptic arrangements of parvocellular, magnocellular, and koniocellular geniculate pathways in owl monkey (Aotus trivirgatus) visual cortex. 1250 10


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