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)

In order to test the proposal that the zona incerta contributes to the generation of orienting movements, we examined the synaptic relationships between the incertotectal pathway and the cells of origin of the predorsal bundle. The predorsal bundle cells give rise to the major premotor pathway from the superior colliculus to the brainstem gaze centers. First, cytochrome oxidase histochemistry, gamma-aminobutyric acid (GABA), and glutamic acid decarboxylase (GAD) immunocytochemistry, and the axonal transport of markers were used to define the borders of a ventral subdivision of the zona incerta. This subdivision projects topographically to the same sublamina of the intermediate grey layer of the superior colliculus that contains the vast majority of the predorsal bundle cells. Experiments in which incertotectal cells were labeled by both retrograde transport and immunocytochemistry showed that this pathway is GABAergic. Retrograde and anterograde experiments also showed that this pathway is reciprocated by a pathway from the intermediate grey layer of the superior colliculus to the same ventral subdivision of the zona incerta. Finally, experiments combining axonal transport and electron microscopic methods showed that the incertotectal pathway is the source of a monosynaptic GABAergic input to the cells of origin of the predorsal bundle. The ventral subdivision of the zona incerta is contrasted with a second source of GABAergic input to the predorsal bundle cells, the substantia nigra pars reticulata.
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PMID:Pathway from the zona incerta to the superior colliculus in the rat. 138 May 19

Increases in immunocytochemically detectable type II calcium-calmodulin-dependent protein kinase (CaM II kinase) and decreases in immunocytochemically detectable glutamic acid decarboxylase (GAD) are known to occur in the visual cortex of adult monkeys following brief periods of monocular visual deprivation. In the present study, GAD and CaM II kinase gene expression was investigated under these conditions. The polymerase chain reaction (PCR) was used to generate species-specific cDNA clones that were used to make antisense RNA probes. A second form of CaM II kinase alpha, CaM II kinase alpha-33, which contains an additional phosphorylation consensus sequence, was identified. In situ hybridization in normal visual cortex revealed a complex sublaminar organization of GAD-expressing cells within layers IVC and VI and a distribution of CaM II kinase alpha-expressing cells that was greatest in layers II, III, IVB, and VI. In situ hybridization in the cortex from animals that had been monocularly deprived revealed enhanced CaM II kinase mRNA levels in deprived-eye columns of layer IVC and, associated with the deprived eye, cytochrome oxidase-stained periodicities in other layers. In layer IV, the enhancement of labeling in deprived-eye stripes was, on average, 16% greater than in normal-eye stripes. By contrast, GAD, mRNA levels appeared unchanged in all layers, suggesting a posttranscriptional regulatory mechanism.
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PMID:Differential effects of monocular deprivation on glutamic acid decarboxylase and type II calcium-calmodulin-dependent protein kinase gene expression in the adult monkey visual cortex. 184 11

The rodent ventrobasal thalamus (VB) contains groups of vibrissa-related neurons (barreloids) that are highly reactive for the enzyme cytochrome oxidase. The present experiments show that each barreloid also contains a dense accumulation of glutamic acid decarboxylase (GAD) immunoreactive terminals. Chronic vibrissa trimming results in parallel declines in staining for both cytochrome oxidase (CO) and GAD in barreloids associated with the trimmed hairs. Thus, thalamic metabolism like that in the cortex is dependent upon normal sensory input. This includes projection neurons as well as neurons in the reticular nucleus, which are the major source of gamma-aminobutyric acid (GABA)ergic input to the rat VB.
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PMID:Chronic sensory deprivation affects cytochrome oxidase staining and glutamic acid decarboxylase immunoreactivity in adult rat ventrobasal thalamus. 244 2

Somatosensory cortex reorganizes following restricted deafferentation so that deprived neurons acquire new receptive fields. Electrophysiological data suggest that a decrease in inhibition might be one of the mechanisms contributing to these changes. This hypothesis was tested by evaluating quantitatively glutamic acid decarboxylase (GAD) immunoreactivity and cytochrome oxidase (CO) activity in normal and partially deafferented rat hindlimb somatosensory cortex. In normal animals, there were laminar differences in the frequencies of GAD+ cells that correlated with the levels of CO activity. Two weeks after transection of the sciatic nerve, CO levels were reduced in all layers of the hindlimb somatosensory cortex contralateral to the nerve transection whereas the frequencies of GAD+ cells were unchanged except in layer IV where a 16% decrease was observed. This observation is consistent with the hypothesis that the expression of GAD in layer IV is partially controlled by the amount of afferent input. The ability of novel inputs to develop stable patterns of excitation in deafferented somatosensory cortex may depend upon the reduction of GABAergic inhibition which follows deafferentation.
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PMID:Quantitative study of glutamic acid decarboxylase-immunoreactive neurons and cytochrome oxidase activity in normal and partially deafferented rat hindlimb somatosensory cortex. 255 82

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

Neuronal cell bodies and synaptic terminals positive for glutamic acid decarboxylase, the enzyme responsible for synthesizing gamma-amino butyric acid, have been located by immunocytochemical staining in all layers of the macaque monkey cortex. In layers II and III the staining pattern of periodic dots is identical with that seen in sections stained for cytochrome oxidase. The rows of dots run parallel with the ocular dominance columns, suggesting that the labelled neurones are preferentially related to each eye.
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PMID:Immunocytochemical localization of glutamic acid decarboxylase in monkey striate cortex. 626 4

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

The postnatal development of direct thalamocortical projections from the zona incerta of the ventral thalamus to the whisker representation area of the rat primary somatosensory cortex was investigated. Cytoarchitectonic analysis based on Nissl staining, cytochrome oxidase histochemistry and immunohistochemistry for glutamic acid decarboxylase, GABA, parvalbumin and calbindin D28K revealed that the zona incerta can be clearly distinguished from surrounding diencephalic structures from the day of birth. Moreover, four distinct anatomical subdivisions of this nucleus were identified: the rostral, dorsal, ventral and caudal. Of these, the ventral subdivision is by far the most conspicuous, containing the highest density of neurons, and the highest levels of cytochrome oxidase, glutamate decarboxylase, GABA, parvalbumin and calbindin D28K. In contrast, the dorsal, rostral and caudal subdivisions contain fewer cells, lower levels of glutamic acid decarboxylase and GABA and very few parvalbumin-positive and calbindin-positive neurons. Small injections of rhodamine coated microspheres or Fluoro-gold in the primary somatosensory cortex of animals at different stages of development revealed the existence of retrogradely labeled neurons in the rostral and dorsal subdivisions of the zona incerta from postnatal day 1. At this age, retrogradely labeled cells were also found in the ventral lateral, ventral posterior medial, posterior medial, centrolateral, ventral medial and magnocellular subdivision of the medial geniculate nuclei of the dorsal thalamus. The density of the incertocortical projection reaches its maximum between the first and second postnatal weeks, decreasing subsequently, until an adult pattern of labeling is achieved. Tracer injections combined with immunohistochemistry revealed that the majority of the incertocortical projection derives from GABAergic neurons, implying a potentially inhibitory role for the incertocortical projection. These results demonstrate that the rat trigeminal system contains parallel thalamocortical pathways of opposite polarity, emerging from both the dorsal (glutamatergic, excitatory) and ventral (GABAergic, inhibitory) thalamus since the day of birth. As such, these findings suggest that, contrary to the classical notion, not only the dorsal but also the ventral thalamus may play a special role in both cortical maturation and function.
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PMID:Development of direct GABAergic projections from the zona incerta to the somatosensory cortex of the rat. 777 73

Much is known about modular organization in the cerebral cortex, but this knowledge is skewed markedly toward primary sensory areas, and in fact, it has been difficult to demonstrate elsewhere. In this report, we test the hypothesis that a unique form of modules exists in the entorhinal area of the human cortex (Brodmann's area 28). We examined this issue using classic cyto- and myeloarchitectonic stains, immunolabeling for various neurochemicals, and histochemistry for certain enzymes. The findings reveal that the entorhinal cortex in the human is formed by a mosaic of cellular aggregates whose most conspicuous elements are the cell islands of layer II and myelinated fibers around the cell islands, the disposition of glutamic acid decarboxylase-positive neurons and processes, cytochrome oxidase staining, and the pattern of cholinergic afferent fibers. The neuropathology of Alzheimer's disease cases highlights the modules, but inversely so, by destroying their features. The findings are of interest because 1) anatomically defined modules are shown to be present in areas other than the sensory and motor cortices, 2) the modules are morphological entities likely to reflect functions of the entorhinal cortex, and 3) the destruction of entorhinal cortex modules may account disproportionately for the severity of memory impairments in Alzheimer's disease.
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PMID:Entorhinal cortex modules of the human brain. 874 6


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