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 periodontal ligament has a rich sensory nerve supply which serves as a sensory apparatus in addition to tooth support. The periodontal ligament contains nociceptors and low-threshold mechanoreceptors. Stimuli applied to teeth evoke various oral reflexes, which make smooth mastication possible via the periodontal mechanoreceptors. Recent morphological and physiological studies have revealed that Ruffini endings, categorized as low-threshold slowly adapting type II (SA II), are essential mechanoreceptors in the periodontal ligament. The periodontal Ruffini endings are ultrastructurally characterized by expanded axon terminals filled with a number of mitochondria and terminal or lamellar Schwann cells. The axon terminals of the periodontal Ruffini endings have finger-like projections, i.e. axonal spines, extending into the surrounding tissue to detect the deformation of collagen fibers. As histochemical marker enzymes for the periodontal Ruffini endings, the axon terminals and terminal Schwann cells are reactive for cytochrome oxidase activity and both acid phosphatase activity and non-specific cholinesterase activity, respectively. Many experimental studies also have revealed that periodontal Ruffini endings have high potential for neuroplasticity, confirmed by intense immunoreactivity for p75-NGFR and GAP-43. Mechanical stimuli due to tooth eruption and occlusion might be a prerequisite for the differentiation and maturation of the periodontal Ruffini endings. Further investigations are needed for clarifying the involvement of growth factors and the molecular mechanism of the development and regeneration processes of the Ruffini endings.
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PMID:[Morphological basis on periodontal Ruffini endings]. 961 78

Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS.
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PMID:Central peptidergic neurons are hyperactive during collateral sprouting and inhibition of activity suppresses sprouting. 1002 46

Vasoactive intestinal polypeptide (VIP) in neocortex affects neuronal excitability as well as cortical blood flow and metabolism. Interneurons immunoreactive for VIP (VIP-IR neurons) are characterized by their predominantly bipolar appearance and the radial orientation of their main dendrites. In order to determine whether the morphology of VIP-IR neurons is related to the functional organization of the cortex into vertical columns, we combined both immunostaining of neurons containing VIP and cytochrome oxidase histochemistry for visualizing barrels, morphological layer IV correlates of functional columns, in the primary somatosensory (barrel) cortex of rats. VIP-IR neurons were localized in supragranular (48%), granular (16%), and infragranular layers (36%) as well as in the white matter. In the granular layer, a clear trend that more neurons were located in interbarrel septa rather than in barrels could be observed, resulting in a neuronal density which was about one-third higher in the septal area. VIP-IR neurons from the different cortical layers were three-dimensionally reconstructed from serial sections by using a computer microscope system. The neurons were mostly bipolar. Striking morphological differences in both axonal and dendritic trees were found between neurons whose cell bodies were located in supragranular, granular, and the upper part of infragranular layers, and those whose cell bodies were located in the area below. The former had dendrites which often reached layer I, where they bifurcated several times, and axonal trees which were particularly oriented vertically, with a tangential extent smaller than the width of barrels. Therefore, these neurons were mostly confined to either a barrel- or septum-related column. By contrast, the dendrites of neurons of the latter group did not reach the granular layer. Furthermore, these neurons had axons with sometimes very long horizontal collaterals, which often spanned two, in one case three, barrel columns. It is proposed that the differential morphology of neurons with different locations as stated above parallels to some extent the divergence of input streaming into the corresponding layer-defined areas. As a possible consequence of this, VIP-IR neurons may be capable of adapting the excitability and metabolism of cortical compartments either in a spatially limited or more extensive way.
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PMID:Neurons immunoreactive for vasoactive intestinal polypeptide in the rat primary somatosensory cortex: morphology and spatial relationship to barrel-related columns. 1075 3

The periodontal ligament receives a rich sensory nerve supply and contains many nociceptors and mechanoreceptors. Although its various kinds of mechanoreceptors have been reported in the past, only recently have studies revealed that the Ruffini endings--categorized as low-threshold, slowly adapting, type II mechanoreceptors--are the primary mechanoreceptors in the periodontal ligament. The periodontal Ruffini endings display dendritic ramifications with expanded terminal buttons and, furthermore, are ultrastructurally characterized by expanded axon terminals filled with many mitochondria and by an association with terminal or lamellar Schwann cells. The axon terminals of the periodontal Ruffini endings have finger-like projections called axonal spines or microspikes, which extend into the surrounding tissue to detect the deformation of collagen fibers. The functional basis of the periodontal Ruffini endings has been analyzed by histochemical techniques. Histochemically, the axon terminals are reactive for cytochrome oxidase activity, and the terminal Schwann cells have both non-specific cholinesterase and acid phosphatase activity. On the other hand, many investigations have suggested that the Ruffini endings have a high potential for neuroplasticity. For example, immunoreactivity for p75-NGFR (low-affinity nerve growth factor receptor) and GAP-43 (growth-associated protein-43), both of which play important roles in nerve regeneration/development processes, have been reported in the periodontal Ruffini endings, even in adult animals (though these proteins are usually repressed or down-regulated in mature neurons). Furthermore, in experimental studies on nerve injury to the inferior alveolar nerve, the degeneration of Ruffini endings takes place immediately after nerve injury, with regeneration beginning from 3 to 5 days later, and the distribution and terminal morphology returning to almost normal at around 14 days. During regeneration, some regenerating Ruffini endings expressed neuropeptide Y, which is rarely observed in normal animals. On the other hand, the periodontal Ruffini endings show stage-specific configurations which are closely related to tooth eruption and the addition of occlusal forces to the tooth during postnatal development, suggesting that mechanical stimuli due to tooth eruption and occlusion are a prerequisite for the differentiation and maturation of the periodontal Ruffini endings. Further investigations are needed to clarify the involvement of growth factors in the molecular mechanisms of the development and regeneration processes of the Ruffini endings.
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PMID:The Ruffini ending as the primary mechanoreceptor in the periodontal ligament: its morphology, cytochemical features, regeneration, and development. 1075 11

This study bears on the projections of layer 5 cells of the vibrissal sensory cortex to the somatosensory thalamus in rats. Small groups of cells were labeled with biotinylated dextran amine (BDA), and their axonal arborizations were individually reconstructed from horizontal sections counterstained for cytochrome oxidase. Results show that the vast majority ( approximately 95%) of layer 5 axons that innervate the somatosensory thalamus are collaterals of corticofugal fibers that project to the brainstem. The anterior pretectal nucleus, the deep layers of the superior colliculus, and the pontine nuclei are among the structures most often coinnervated. In the thalamus, layer 5 axons terminate exclusively in the dorsal part of the posterior group (Po), where they form clusters of large terminations. Because dorsal Po projects to multiple cortical areas, we sought to determine whether all recipient areas return a layer 5 projection to this part of the thalamus. Additional experiments using fluoro-gold and BDA injections provided evidence that the primary somatosensory area is the sole source of layer 5 projections to dorsal Po but that this thalamic region receives convergent layer 6 projections from the primary and second somatosensory areas and from the motor and insular cortices. These results show that layer 5 projections do not overlap in associative thalamic nuclei, thus defining area-related subdivisions. Furthermore, the coinnervation of brainstem nuclei by layer 5 CT axons suggests that this pathway conveys to the thalamus a copy of the cortical output aimed at brainstem structures.
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PMID:Corticothalamic projections from layer 5 of the vibrissal barrel cortex in the rat. 1090 97

Cytochrome oxidase, the terminal enzyme of the electron transport chain, is a marker of the functional activity of the cell. In this study; localization of cytochrome oxidase in cerebrum, cerebellum, hippocampus, substantia nigra and choroid plexus of adult rats was investigated using immunohistochemical methods. Neural bodies were immunoreactive while neuroglial cells and axonal areas did not show significant immunostaining. The cerebral cortical substantia grisea region was stained almost homogeneously with cytochrome oxidase. In the cerebellar cortex, immunolabelling was more intense in the granular layer than the molecular layer. There was significant immunostaining in Purkinje cells. White matter, both in cerebrum and cerebellum, did not show immunoreactivity for cytochrome oxidase. Neurones in the hippocampus showed variable immunostaining; some of them were negative while others revealed high immunoreactivity. The neurones in substantia nigra were heavily labelled. Immunostaining for cytochrome oxidase in plexus choroideus epithelial cells was also remarkable. The morphological findings demonstrate the regions which most require and produce energy and reflect the differences in cellular activity in these parts of the central nervous system.
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PMID:Immunohistochemical demonstration of cytochrome oxidase in different parts of the central nervous system: a comparative experimental study. 1119 78

Patients treated with nucleoside analogue reverse transcriptase inhibitors (NRTIs) develop a varying degree of myopathy or neuropathy after long-term therapy. Zidovudine (AZT) causes myopathy; zalcitabine (ddC), didanosine (ddl) and lamuvidine (3TC) cause neuropathy; stavudine (d4T) and fialuridine (FIAU) cause neuropathy or myopathy and lactic acidosis. The tissue distribution of phosphorylases responsible for phosphorylation of NRTIs relates to their selective tissue toxicity. The myopathy is characterized by muscle wasting, myalgia, fatigue, weakness and elevation of CK. The neuropathy is painful, sensory and axonal. In vitro, NRTIs inhibit the gamma-DNA polymerase, responsible for replication of mtDNA, and cause mtDNA dysfunction. In vivo, patients treated with AZT, the best studied NRTI, develop a mitochondrial myopathy with mtDNA depletion, deficiency of COX (complex IV), intracellular fat accumulation, high lactate production and marked phosphocreatine depletion, as determined with in vivo MRS spectroscopy, due to impaired oxidative phosphorylation. Animals or cultured cells treated with NRTIs develop neuropathy, myopathy, or cell destruction with similar changes in the mitochondria. There is evidence that the NRTI-related neuropathy is also due to mitochondrial toxicity. The NRTIs (AZT, ddC, ddl, d4T, 3TC) contain azido groups that compete with natural thymidine triphosphate as substrates of DNA pol-gamma and terminate mtDNA synthesis. In contrast, FIAU that contains 3'-OH groups serves as an alternate substrate for thymidine triphosphate with DNA pol-gamma and is incorporated into the DNA causing permanent mtDNA dysfunction. The NRTI-induced mitochondrial dysfunction has an influence on the clinical application of these agents, especially at high doses and when combined. They have produced in humans a new category of acquired mitochondrial toxins that cause clinical manifestations resembling the genetic mitochondrial disorders.
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PMID:Peripheral neuropathy and antiretroviral drugs. 1129 2

Activity levels of cytochrome oxidase, acid phosphatase, and NADPH diaphorase were examined in the perikarya of immunohistochemically identified Renshaw cells from sections of rat lumbar spinal cord. Renshaw cell profiles were identified on the basis of their characteristic anti-gephyrin-immunofluorescent labelling. Intrasomatic densities of enzyme histochemical reaction product were employed as indicators of relative mitochondrial activity (cytochrome oxidase), intracytoplasmic digestion (acid phosphatase), or putative nitrergic signalling (NAPDH-diaphorase). Approximately half of the Renshaw cell somata examined displayed moderate levels of cytochrome oxidase reaction product (142 of 262 Renshaw cells) or low levels of acid phosphatase activity (156 of 243 Renshaw cells). A majority (160 of 202 cells) of Renshaw cells contained low intrasomatic levels of NADPH-diaphorase activity but most of these cells were closely apposed by at least one NADPH-diaphorase reactive axonal varicosity. Our findings suggest that moderate levels of perikaryal oxidative metabolism and low levels of intracytoplasmic digestion are sufficient for, and support, the unique physiological capabilities of Renshaw cells. The presence of NADPH-diaphorase containing somatic close contacts indicate that nitric oxide may have at least a minor role in the regulation of Renshaw cell activity. These results are complementary and consistent with previous morphological and pharmacological demonstrations of Renshaw cell heterogeneity.
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PMID:Enzyme histochemical profile of immunohistochemically identified Renshaw cells in rat lumbar spinal cord. 1140 94

The CNS contains high levels of the glycosaminoglycan hyaluronan, and neural cells express a variety of proteins that are members of the hyaladherin family of hyaluronan-binding proteins. We have previously shown that the hyaladherin RHAMM (receptor for hyaluronan-mediated motility; CD168) is expressed by neural cells in culture; plays a role in astrocyte motility, neurite migration, and axonal growth; and is widely distributed in neurons and oligodendrocytes of developing and adult rat CNS. Here we demonstrate differential localization of various forms of RHAMM in subcellular fractions of adult rat brain. Western blotting indicated the presence of 66, 75, and 85-90 kDa molecular weight RHAMM forms in whole-brain homogenates. Subfractionation revealed enrichment of the 66 and 85-90 kDa forms in soluble fractions, whereas the 75 kDa form was enriched in mitochondrial fractions. This latter form was retained in osmotically shocked mitochondria, but was liberated by alkali carbonate, suggesting a nonintrinsic mitochondrial membrane association. By double immunohistochemical labeling for RHAMM and the mitochondrial marker cytochrome oxidase, RHAMM was localized to isolated mitochondria in vitro and to neuronal mitochondria in vivo. Hyaluronan-sepharose chromatography and cetylpiridinium chloride precipitation confirmed the hyaluronan-binding capacity of RHAMM forms. By calmodulin-affinity chromatography, endogenously expressed brain RHAMM was demonstrated to bind calmodulin in a Ca2+-dependent manner. These results, together with reports of RHAMM association with actin and microtubules in other systems, suggest a role of RHAMM in calmodulin-mediated cell signaling to cytoskeletal elements and/or mitochondria in the CNS and invoke novel functions of its interactions with hyaluronan.
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PMID:Subcellular distribution, calmodulin interaction, and mitochondrial association of the hyaluronan-binding protein RHAMM in rat brain. 1143 24

Cortical strokes alter functional maps but associated changes in connections have not been documented. The neuroanatomical tracer biotinylated dextran amine (BDA) was injected into cortex bordering infarcts 3 weeks after focal strokes in rat whisker barrel (somatosensory) cortex. The mirror locus in the opposite hemisphere was injected as a control. After 1 week of survival, brains were processed for cytochrome oxidase (CO)-, Nissl-, and BDA-labeled neurons. Cortex bordering the infarct (peri-infarct cortex) had abnormal CO and Nissl structure. BDA-labeled neurons were plotted and projections were analyzed quantitatively. Animals with small strokes had intracortical projections, arising from peri-infarct cortex, not seen in normal hemispheres: the overall orientation was statistically significantly different from and rotated 157 degrees relative to the controls. Compared to the controls, significantly fewer cells were labeled in the thalamus. Thus, after focal cortical stroke, the peri-infarct cortex is structurally abnormal, loses thalamic connections, and develops new horizontal cortical connections by axonal sprouting.
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PMID:New patterns of intracortical projections after focal cortical stroke. 1159 58


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