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)

Immunocytochemical techniques were used to investigate the distribution of gamma-aminobutyric acidA (GABAA) receptors in the rat primary somatosensory cortex (SI). Monoclonal antibody 62-3G1 (de Blas et al., 1988; Victorica et al., 1988), which recognizes an epitope common to the beta 2 and beta 3 subunits of the GABAA receptor, produces staining of small punctate structures throughout the neuropil, and around somata and linear processes in all laminae of SI. Receptor immunostaining is relatively intense in upper lamina I and in lamina IV, where patches of intense receptor staining are interleaved with narrow zones of moderate immunoreactivity. Staining is lightest in lamina Vb, where stained puncta appear to be aligned with radially oriented processes, and moderate in the remaining laminae. Tangential sections through lamina IV reveal that each large cortical barrel encompasses several patches of intense receptor staining that are aligned with the corners or edges of individual barrels; interbarrel septa are moderately of intense cytochrome oxidase (CO) histochemical staining. A similar correspondence is apparent between a complex lattice of dense receptor clustering and a plexus of dark CO staining in the cortical trunk representation. Six to eight weeks of tactile deprivation produced by simple whisker trimming have no visible effect on GABAA receptor distribution. This is the case for rats whose whiskers were trimmed only during adulthood and for rats deprived from the day of birth until examination 6-8 weeks later. However, electrocautery ablation of whisker follicles leads to a marked decline in GABAA receptor immunoreactivity in cortical barrels associated with the ablated follicles. Our findings indicate that there is reasonable, though not perfect, correspondence between the distribution of GABAA receptors and the distribution of GABA-containing neurons and terminals in rat SI. These elements are associated with regions of intense oxidative metabolic activity revealed by CO staining. The density of GABAA receptors is reduced in lamina IV following complete loss of peripheral afferent input. However, less severe tactile deprivation, which is known to affect cortical neuron responsiveness, produces little or no change in receptor distribution.
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PMID:Immunocytochemical localization of GABAA receptors in rat somatosensory cortex and effects of tactile deprivation. 750 3

Monospecific antibodies to glutamate were used to characterize the organization of excitatory neurons and the plasticity of glutamate expression in the macaque striate cortex. Somata and processes immunoreactive for glutamate were densely and unevenly distributed in layers II-III, IVA, IVC. In tangential sections through layers II and III, patches of intense glutamate immunostaining were observed and were found to coincide with regions of the cytochrome oxidase (CO)-rich puffs. By contrast, clusters of intense immunostaining were surrounded by the lightly immunostained but intensely CO-stained lattice in layer IVA. Similarly, in layer IVC, focal aggregates of intense glutamate immunoreactivity were interspersed among regions of light immunostaining but intense CO staining. Glutamate immunoreactivity was also intense in layer VI but was much lighter in layers I, IVB, and V. Throughout the striate cortex, neurons resembling pyramidal cells and spiny stellate cells and processes that included dendrites and axons were immunostained. None of the glutamate-positive neurons was GABA immunoreactive. Following monocular deprivation of adult monkeys by intravitreal injections of TTX into one eye, glutamate immunoreactivity in layers IVC was distributed in alternating intensely and lightly stained stripes. The stripes of reduced immunostaining, which contained an abnormally low concentration of glutamate neurons and pale neuropil, corresponded to columns dominated by the TTX-injected eye. Similar stripes of alternating intense and light immunoreactivity were seen in layers II-III, where they corresponded to rows of puffs at the centers of intact-eye and deprived-eye columns, respectively. These findings demonstrate that glutamate-immunoreactive neurons and terminals in monkey striate cortex are densely concentrated in layers receiving direct geniculocortical innervation. In addition, the glutamate neurons and terminals form discrete units, which in layers II and III coincide precisely with regions receiving geniculocortical terminations but in layers IVA are segregated from these terminations. The findings also indicate that glutamate immunoreactivity is regulated by visually driven activity, and suggest that monocular deprivation in adulthood leads to a reduction in the major excitatory neurotransmitter in visual cortex as well as previously indicated reductions in GABA, the major inhibitory neurotransmitter.
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PMID:Neuronal characterization, compartmental distribution, and activity-dependent regulation of glutamate immunoreactivity in adult monkey striate cortex. 750 64

Sodium azide is an inhibitor of cytochrome oxidase which produces selective striatal lesions in both rodents and primates. In the present study we investigated the neurochemical and histologic effects of both intrastriatal and systemic administration of sodium azide, as well as the age dependence and mechanism of the lesions. Intrastriatal administration of sodium azide produced dose-dependent lesions. Neurochemical and histologic evaluation showed that markers of both spiny projection neurons (GABA, substance P) and aspiny interneurons (somatostatin, neuropeptide Y, NADPH-diaphorase) were equally affected. Subacute systemic administration of sodium azide resulted in lesions with a similar neurochemical profile; however, in contrast to intrastriatal injections there was sparing of dopaminergic striatal afferents. Prior decortication significantly attenuated lesions produced by intrastriatal administration of sodium azide, consistent with an excitotoxic process. Chronic administration of sodium azide for 1 month lead to striatal neuropathological changes. Lesions produced by intrastriatal administration of sodium azide in 1-, 4-, and 12-month-old animals showed age dependence. Both freeze-clamp measurements and chemical-shift magnetic resonance spectroscopy confirmed that sodium azide impairs oxidative phosphorylation in the striatum following either intrastriatal or systemic administration. These results show that the striatum is particularly vulnerable to oxidative stress produced by sodium azide, and that it produces striatal lesions by a secondary excitotoxic mechanism.
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PMID:Systemic or local administration of azide produces striatal lesions by an energy impairment-induced excitotoxic mechanism. 752 31

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

Seven monkey-specific GABAA receptor subunit cDNAs were isolated and cloned; radioactive cDNA and cRNA probes derived from them were used for Northern blot analysis and in situ hybridization histochemistry of the primary visual cortex (area 17), with comparative observations on other cortical areas. cDNAs corresponding to alpha 1, alpha 2, alpha 4, alpha 5, beta 1, beta 2, and gamma 2 GABAA receptor subunits were isolated and had sequences unique to the monkey but recognized mRNAs of distinct molecular weights consistent with those reported in other species. mRNAs for the alpha 1, beta 2, and gamma 2 subunits were expressed at much higher levels in area 17 than in motor, somatosensory, or temporal association cortex, possibly reflecting the greater density of GABA cells and synapses in area 17. In areas 17 and 18, each of the seven subunit mRNAs showed individually distinct patterns of laminar distribution. alpha 1, beta 2, and gamma 2 subunit mRNAs, which are thought to form the basis of receptors with the full range of classical GABAA receptor properties in the adult, were particularly enriched in layers II-III, IVC, and VI of area 17, following patterns of receptor distribution previously demonstrated by radioligand binding and immunocytochemistry. alpha 2, alpha 4, alpha 5, and beta 1 transcripts had quite different localization patterns that did not match the antoradiographic or immunocytochemical receptor localization patterns. alpha 2 and alpha 5 subunit mRNAs, which are thought to be the subunits mainly expressed in development, were enriched in layer VI and the underlying white matter, possibly reflecting the involvement of receptors formed from alpha 2 and alpha 5 polypeptides in trophic interactions in the cortical subplate zone during development of the cerebral cortex. Following 8-21 d periods of monocular deprivation induced by intravitreal injection of TTX, levels of alpha 1, beta 2, and gamma 2 subunit mRNAs were substantially reduced in deprived ocular dominance columns of layer IVC in area 17. The effect was greatest for the alpha 1 subunit; for both alpha 1 and gamma 2 subunit mRNAs, it extended into deprived rows of cytochrome oxidase-identified periodicities in other layers. Apart from the alpha 5 subunit mRNA, which showed reduced levels in layer VI, the other subunit mRNAs were unaffected by monocular deprivation. These results demonstrate the heterogeneity of GABAA receptor subunit expression in a complex, multilaminar cortical area. They suggest that receptors with different functional properties may be assembled from different combinations of subunit polypeptides in different layers and show that subunit expression is differentially regulated under activity-dependent conditions.
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PMID:Lamina-specific expression and activity-dependent regulation of seven GABAA receptor subunit mRNAs in monkey visual cortex. 815 67

Subunit proteins that make up functional GABAA receptors were localized immunocytochemistry in the primary visual cortex (area 17) of adult monkeys and humans. Immunoreactivity for the alpha 1, beta 2/3, and gamma 2 subunits is greatest in layers (II-III, IVA and IVC) of monkey area 17 that contain the highest density of GABA neurons and terminals. Immunostaining for each subunit is unevenly distributed in layers II and III, where patches of immunoreactivity correspond to regions of intense cytochrome oxidase (CO) staining, and in layer IVA, where intense immunoreactivity forms a honeycomb pattern identical to the CO staining pattern. Immunoreactivity for the subunits is localized principally within the neuropil, which, by simultaneous comparison with the distribution of microtubule-associated protein immunostaining, was found to include bundles of thin dendrites and zones of numerous dendritic segments. In addition, gamma 2 immunostaining surrounds the somata of a subpopulation of GABAergic neurons, immunoreactive for the calcium-binding protein parvalbumin. All three subunits are present in the somata and processes of neurons that occupy the white matter subjacent to monkey area 17. In human visual cortex, the alpha 1, beta 2/3, and gamma 2 subunits are distributed in a manner similar to that found in monkeys, with relatively intense immunostaining in layers IVC and IVA. In layer IVC, vertical stripes of intense receptor immunostaining (20-30 microns wide) alternate with wider stripes of pale immunostaining (30-60 microns wide). In the upper and lower halves of IVC beta, these stripes form lattices similar to those in layers IVC and IVA of monkeys. Following monocular deprivation by intravitreal injections of TTX in adult monkeys, immunoreactivity for each subunit in layer IVC consists of alternating intensely and lightly stained stripes. Comparison with the pattern of CO staining indicates that intense immunostaining for alpha 1, beta 2/3, and gamma 2 occurs in normal-eye stripes while abnormally light immunostaining is present in deprived-eye stripes. For all three subunits, immunoreactivity in deprived-eye stripes is reduced within 5 d of monocular deprivation and remains abnormally low for deprivations that extend to at least 30 d. These findings indicate that each of several GABAA receptor subunits adopt similar laminar and compartmental distributions in monkey and human area 17 and are likely to be expressed by the same neurons. The deprivation-dependent reduction in immunoreactivity for alpha 1, beta 2/3, and gamma 2 subunits suggests that all are regulated by visually driven activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:GABAA receptor subunit immunoreactivity in primate visual cortex: distribution in macaques and humans and regulation by visual input in adulthood. 815 75

Monocular deprivation produces an imbalance in visual drive from the two eyes, which in adult macaque V1 leads to marked changes in the neurochemistry of GABA interneurons. Such changes were further examined by studying immunoreactivity for calbindin, calretinin, and parvalbumin, three calcium-binding proteins that mark distinct subpopulations of GABA neurons, in macaques that had been monocularly deprived by intravitreal injection of tetrodotoxin. Deprivation for 5 d or longer produced a reversal in the normal pattern of calbindin immunostaining in layer III, from one in which intense neuronal immunostaining surrounded the cytochrome oxidase-rich puffs to one in which it occupied the puffs. Over the same period, calbindin immunostaining in other layers was reduced across the entire width of deprived-eye columns or extended into flanking regions of normal-eye columns. In contrast, reduction in parvalbumin immunostaining occurred only in deprived-eye columns and included only terminals with short periods of deprivation (up to 17 d) but both terminals and somata with longer periods. No change in calretinin immunoreactivity was observed. These findings demonstrate that GABA neurons of macaque V1 vary in their response to monocular deprivation according to their neurochemistry and position, suggesting that the weight of inputs from the two eyes and the intrinsic characteristics of each GABA population determine how a neuron responds to a change in visual input.
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PMID:Regulation of calcium-binding protein immunoreactivity in GABA neurons of macaque primary visual cortex. 867 Jun 56

One of the hallmarks of the primate striate cortex is the presence of cytochrome oxidase (CO)-rich puffs and CO-poor interpuffs in its supragranular layers. However, the neurochemical basis for their differences in metabolic activity and physiological properties is not well understood. The goals of the present study were to determine whether CO levels in postsynaptic neuronal compartments were correlated with the proportion of excitatory glutamate-immunoreactive (Glu-IR) synapses they received and if Glu-IR terminals and synapses in puffs differed from those in interpuffs. By combining CO histochemistry and postembedding Glu immunocytochemistry on the same ultrathin sections, the simultaneous distribution of the two markers in individual neuronal profiles was quantitatively analyzed. As a comparison, adjacent sections were identically processed for the double labeling of CO and GABA, an inhibitory neurotransmitter. In both puffs and interpuffs, most axon terminals forming asymmetric synapses (84%)--but not symmetric ones, which were GABA-IR--were intensely immunoreactive for Glu. GABA-IR neurons received mainly Glu-IR synapses on their cell bodies, and they had three times as many mitochondria darkly reactive for CO than Glu-rich neurons, which received only GABA-IR axosomatic synapses. In puffs, GABA-IR neurons received a significantly higher ratio of Glu-IR to GABA-IR axosomatic synapses and contained about twice as many darkly CO-reactive mitochondria than those in interpuffs. There were significantly more Glu-IR synapses and a higher ratio of Glu- to GABA-IR synapses in the neuropil of puffs than of interpuffs. Moreover, Glu-IR axon terminals in puffs contained approximately three times more darkly CO-reactive mitochondria than those in interpuffs, suggesting that the former may be synaptically more active. Thus, the present results are consistent with our hypothesis that the levels of oxidative metabolism in postsynaptic neurons and neuropil are positively correlated with the proportion of excitatory synapses they receive. Our findings also suggest that excitatory synaptic activity may be more prominent in puffs than in interpuffs, and that the neurochemical and synaptic differences may constitute one of the bases for physiological and functional diversities between the two regions.
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PMID:Differential glutamatergic innervation in cytochrome oxidase-rich and -poor regions of the macaque striate cortex: quantitative EM analysis of neurons and neuropil. 876 29

Electrophysiological data from the rodent whisker/barrel cortex indicate that GABAergic, presumed inhibitory, neurons respond more vigorously to stimulation than glutamatergic, presumed excitatory, cells. However, these data represent very small neuronal samples in restrained, anesthetized, or narcotized animals or in cortical slices. Histochemical data from primate visual cortex, stained for the mitochondrial enzyme cytochrome oxidase (CO) and for GABA, show that GABAergic neurons are more highly reactive for CO than glutamatergic cells, indicating that inhibitory neurons are chronically more active than excitatory neurons but leaving doubt about the short-term stimulus dependence of this activation. Taken together, these results suggest that highly active inhibitory neurons powerfully influence relatively inactive excitatory cells but do not demonstrate directly the relative activities of excitatory and inhibitory neurons in the cortex during normal behavior. We used a novel double-labeling technique to approach the issue of excitatory and inhibitory neuronal activation during behavior. Our technique combines high-resolution 2-deoxyglucose (2DG), immunohistochemical staining for neurotransmitter-specific antibodies, and automated image analysis to collect the data. We find that putative inhibitory neurons in barrel cortex of behaving animals are, on average, much more heavily 2DG-labeled than presumed excitatory cells, a pattern not seen in animals anesthetized at the time of 2DG injection. This metabolic activation is dependent specifically on sensory inputs from the whiskers, because acute trimming of most whiskers greatly reduces 2DG labeling in both cell classes in columns corresponding to trimmed whiskers. Our results provide confirmation of the active GABAergic cell hypothesis suggested by CO and single-unit data. We conclude that strong activation of inhibitory cortical neurons must confer selective advantages that compensate for its inherent energy inefficiency.
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PMID:GABAergic neurons in barrel cortex show strong, whisker-dependent metabolic activation during normal behavior. 920 33

Studies were undertaken to determine whether neurons of the subplate layer represent a transient or stable population of cells in developing neocortex of rat. The first set of studies sought to determine the fraction of subplate neurons that is lost during early postnatal development. The optical dissector method was used to analyze fluorescently stained material in animals the age of postnatal day 0 (P0) to P40. These results demonstrate a reduction of slightly less than half of the total number of subplate neurons from P0 to P40. Counts of labeled cells in littermates at varied ages after [(3)H]thymidine or BRDU treatment on gestational day 14 (G14 - birthdate of occipital subplate neurons) or G18 (birthdate of layers III-IV neurons) demonstrate loss of approximately 50% of neurons in the subplate layer between P0 and P40, somewhat greater than the loss of neurons from cortical layers III-IV. The second set of studies investigated whether subplate neurons display cellular atrophy during postnatal development. Analysis of subplate neurons injected intracellularly with Lucifer yellow in fixed slice preparations indicates no reduction in soma size, number of dendrites, or extent of dendritic fields of subplate neurons taken from animals age P0 to P60. The third set of studies investigated whether functional markers of subplate neurons are reduced during postnatal development. Analysis of tissue stained histochemically for cytochrome oxidase or acetylcholinesterase, or stained immunocytochemically for GABA, somatostatin, or neuropeptide Y, demonstrate a remarkable loss of expression of staining patterns from late gestational ages to P20. These data demonstrate that, although subplate neurons seem not to be a transient population of cells in the usual sense of being eliminated by cell death or structural atrophy, the loss of histochemical and immunocytochemical markers indicates that they may be a functionally transient population of cells.
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PMID:Do subplate neurons comprise a transient population of cells in developing neocortex of rats? 1102 4


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