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 striatum and the mesencephalic dopamine neurons which innervate it, are each organized into developmentally and biochemically distinct compartments. Striatal patches, characterized in the neonate by high concentrations of opiate receptors and substance P, are innervated prenatally by fibers originating in one group of midbrain dopamine neurons, the ventral tier. By the third postnatal day, a dense dopamine projection from neurons in the dorsal tier of the mesostriatal group innervates non-patch areas of the striatum, i.e. the matrix, and is followed by the appearance there of neurotensin, somatostatin and calcium binding protein. We have recently observed that the period of establishment of connections between dorsal tier dopamine neurons and their target cells in the striatal matrix is accompanied by a surge in expression of the gene coding for tyrosine hydroxylase (TH). In order to determine the overall metabolic state of mesencephalic and striatal neurons during the period of up-regulation of TH gene expression, we have applied immunocytochemistry for neuron specific enolase (NSE), and cytochrome oxidase histochemistry, known markers for neuronal activity, as well as TH immunohistochemistry to the mesencephalon and striatum of postnatally developing rats. At birth, both NSE and cytochrome oxidase were expressed almost exclusively in the patches, appearing in the matrix only after the 2nd postnatal day. Patches of NSE remained visible thru the 14th day. In the mesencephalon, cytochrome oxidase and immunoreactive NSE cells in adjacent sections, were present only in the pars reticulata (i.e. ventral tier). By day 8, both techniques identified nigral cells in the dorsal as well as ventral tiers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Temporal and compartmental restriction of neuron-specific enolase expression in the rat mesostriatal system. 133 Mar 70

Endogenous cytochrome oxidase activity was investigated in the adult rat striatum at the light microscope level to see if it was distributed in accordance with the established striatal patch/matrix compartmentalisation. Striatal sections stained to visualise cytochrome oxidase activity were compared with serial sections stained to visualise tyrosine hydroxylase and calbindinD28k-like immunoreactivity, established markers of the matrix compartment. The distribution of endogenous cytochrome oxidase activity was found to coincide with the immunocytochemical staining pattern seen for tyrosine hydroxylase and calbindinD28k whereby areas of intense tyrosine hydroxylase and calbindinD28k-like immunoreactivity (termed the matrix) corresponded to areas of intense cytochrome oxidase activity. Conversely, areas of less intense tyrosine hydroxylase and calbindinD28k-like immunoreactivity (termed patches) corresponded to areas of low cytochrome oxidase activity. In addition, the distribution of two other oxidative enzymes involved in the regulation of mitochondrial respiration, succinic dehydrogenase and NADH-diaphorase, was examined in the striatum and substantia nigra by using histochemical techniques. Both NADH-diaphorase and succinic dehydrogenase histochemistry showed an uneven pattern of neuropil staining in the striatum. In the substantia nigra a few intensely stained cell bodies were seen in the dorsal-lateral tip of the pars reticulata with both histochemical techniques. By using an anti-cytochrome oxidase antibody an abundance of immunoreactive cell bodies and processes were seen in the substantia nigra, particularly in the dorso-medial rim and dorsal tip of the pars reticulata. The substantia nigra pars lateralis contained many intensely stained cytochrome oxidase-like immunoreactive cell bodies and processes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Compartmental distribution of cytochrome oxidase in the striatum of the rat. 134 42

Intrastriatal transplantation of fetal striatal (STR), cortical (CTX), or ventral mesencephalic (VM) tissue into the normal striatum has been shown to produce behavioral deficits (38). Here, we have examined the cellular elements of the transplants and their connectivity with the host using histochemistry for cytochrome oxidase (CO) and acetylcholinesterase (AChE), immunocytochemistry for glial fibrillary acidic protein (GFAP), OX42, tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), serotonin (5-HT), and cholecystokinin (CCK). Autoradiography for dopamine D1 and D2, muscarinic cholinergic, and serotonin 5-HT1 and 5-HT2 receptors at 5-15 months after transplantation was also investigated. CO staining showed that all transplants were metabolically active. The STR and VM transplants contained AChE-positive neurons and fibers. The CTX transplants exhibited AChE terminals with an appearance similar to that of the host cortex. AChE staining within the STR transplants was patchy. 5-HT-, TH-, and DBH-immunoreactive (IR) fibers were found in the STR and CTX transplants. In two of six CTX transplants, many TH-IR neurons were present. The VM transplants contained many TH-IR, 5-HT-IR, and DBH-IR cell bodies and fibers. CCK-IR stain was found in the VM transplant and was coextensive with regions containing TH-IR cell bodies. Fibers stained by all markers crossed the transplant and host border. Receptor autoradiography revealed that muscarinic cholinergic and 5-HT2 receptors were present in the STR, CTX, and VM transplants. In addition, dopamine D1 and D2 receptors were present in the STR transplants. Intermittent heavy staining for GFAP and OX42 were observed along the border of most transplants and the hosts. It was noted that high densities and hypertrophy of GFAP- or OX42-stained astrocytes or microglia, respectively, were present in the transplants and adjacent host. OX42-stained macrophages were found in many transplants. The present results indicate that intrastriatal transplants into the intact normal brain express numerous histochemical, immunocytochemical, and receptor features characteristic of the appropriate adult tissues. The afferents from the host extend into the STR and CTX transplants, and neural fibers from the VM transplants grew into surrounding host tissue, suggesting possible anatomical connection. Ultrastructural evidence is needed to determine if these fibers form synaptic connections. The results from GFAP and OX42 immunocytochemical staining support the possibility suggested by behavioral studies that damage to the host brain is induced by neural transplantation.
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PMID:Striatal, ventral mesencephalic and cortical transplants into the intact rat striatum: a neuroanatomical study. 165 Dec 54

In order to determine the changes in gonadotrophin releasing hormone (GnRH) and dopaminergic activity within the brain during the onset of sexual precocity, a Halasz-like knife was developed to produce discrete parasagittal cuts in 2-week-old male broiler chicks. At 5 weeks of age, sexually precocious respondents were selected on the basis of advanced secondary sex characteristics and randomly paired with sham-operated controls. Each pair of birds was perfused with heparinized saline followed by 4% paraformaldehyde. Sections 40 microns thick, obtained throughout the hypothalamus, were immunostained with either anti-GnRH or anti-tyrosine hydroxylase (TH) to ascertain dopaminergic activity. Alternate sections from each pair of brains were also treated with cytochrome oxidase to determine metabolic activity levels or with Nissl stain to localize the knife cuts. Analysis revealed an increase in GnRH immunoreactivity within the bed nucleus of the pallial commissure (nCPa) and paraventricular nucleus (PVN), as well as the median eminence (ME). An increase in TH immunoreactivity was observed in the nucleus intramedialis (nI). Also an increase in metabolic activity was seen in the PVN as revealed by cytochrome oxidase reactivity. It is hypothesized that during the onset of puberty there is an increase in immunoreactive GnRH cell numbers as a result of a decrease in the inhibition of the GnRH system, possibly involving the nI and PVN. The source of the dopamine reported in the ME could be from the nI and other nearby nuclei. Dopamine from the tubero-infundibular area may be one of the putative neurotransmitters responsible for the increased activity of GnRH within the ME of chicks showing precocious puberty.
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PMID:Immunocytochemical and histochemical analyses of gonadotrophin releasing hormone, tyrosine hydroxylase, and cytochrome oxidase reactivity within the hypothalamus of chicks showing early sexual maturation. 809 25

A patient with Parkinson's disease received bilateral fetal human nigral implants from six donors aged 6.5 to 9 weeks post-conception. Eighteen months following a post-operative clinical course characterized by marked improvement in clinical function, this patient died from events unrelated to the grafting procedure. Post-mortem histological analyses revealed the presence of viable grafts in all 12 implant sites, each containing a heterogeneous population of neurons and glia. Approximately 210,146 implanted tyrosine hydroxylase-immunoreactive (TH-ir) neurons were found. A greater number of TH-ir grafted neurons were observed in the right (128,162) than the left (81,905) putamen. Grafted TH-ir neurons were organized in an organotypic fashion. These cells provided extensive TH-ir and dopamine transporter-ir innervation to the host striatum which occurred in a patch-matrix fashion. Quantitative evaluations revealed that fetal nigral grafts reinnervated 53% and 28% of the post-commissural putamen on the right and left side, respectively. Grafts on the left side innervated a lesser area of the striatum, but optical density measurements were similar on both sides. There was no evidence that the implants induced sprouting of host TH-ir systems. Electron microscopic analyses revealed axo-dendritic and occasional axo-axonic synapses between graft and host. In contrast, axo-somatic synapses were not observed. In situ hybridization for TH mRNA revealed intensely hybridized grafted neurons which far exceeded TH mRNA expression within residual host nigral cells. In addition, gamma-amino butyric acid (GABA)-ergic neurons were observed within the graft that formed a dense local neuropil which was confined to the implant site. Serotonergic neurons were not observed within the graft. Cytochrome oxidase activity was increased bilaterally within the grafted post-commissural putamen, suggesting increased metabolic activity. In this regard, a doubling of cytochrome oxidase activity was observed within the grafted post-commissural putamen bilaterally relative to the non-grafted anterior putamen. The grafts were hypovascular relative to the surrounding striatum and host substantia nigra. Blood vessels within the graft stained intensely for GLUT-1, suggesting that this marker of blood--brain barrier function is present within human nigral allografts. Taken together, these data indicate that fetal nigral neurons can survive transplantation, functionally reinnervate the host putamen, establish synaptic contacts with host neurons, and sustain many of the morphological and functional characteristics of normal nigral neurons following grafting into a patient with PD.
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PMID:Functional fetal nigral grafts in a patient with Parkinson's disease: chemoanatomic, ultrastructural, and metabolic studies. 880 31

Previous studies have documented a highly compartmentalized and laminar organization of dopamine D2 receptors in human hippocampus, entorhinal and perirhinal cortices. These areas receive input from regions of polysensory association cortices of the superior and inferior temporal sulci that evidence functional modules identified by other techniques. We examined the isocortical regions of temporal lobe for an equally well-differentiated pattern of D2 receptor expression as observed in their paleocortical temporal lobe targets. Using quantitative autoradiography we identified an organization of three-dimensional bands of high concentrations of dopamine D2 receptors throughout the rostral-caudal extent of the normal human temporal cortex. In the coronal plane, these D2 receptor-enriched bands had a columnar appearance with the concentration of D2 receptors almost two-fold higher within the bands than in the immediately adjacent cortex. These D2 receptor-enriched bands had a distinct laminar appearance with a paucity of [125I]epidepride binding to D2 receptors over the granule cell layer and higher concentrations of D2 receptors in laminae III and V than in the immediately adjacent cortex. They had a consistent width (mean width of 2.83 +/- 0.62 mm) in the coronal plane, but had their long axes in the rostrocaudal plane (some were at least 2500 microns in length). Hence, they exist as three-dimensional D2 receptor-enriched and receptor-poor modules with their long axes in the rostrocaudal plane. Tyrosine hydroxylase-immunoreactive fibers were observed to cross orthogonally to the long axes of the D2 receptor enriched bands. Other monoamine receptors (beta-adrenergic, 5-hydroxytryptamine2), and markers for myelin (anti-myelin basic protein immunohistochemistry), glia (5'-nucleotidase), and energy metabolism (cytochrome oxidase) showed a laminar organization but failed to demarcate the D2 receptor-enriched bands. The majority of these D2 receptor-enriched bands were observed in the lateral and inferior aspects of the superior temporal gyrus, less frequently on the lateral surface of the inferior temporal gyrus and the parahippocampal cortices (Brodmann's area 22, 42 and 20, 21, 37). They were absent from primary auditory cortex (Brodmann's 41). The present study is the first known observation of a modular organization of synaptic elements, identified by D2 receptors, in non-primary sensory cortices of any species. The dopamine D2 receptor-enriched bands were found in regions previously identified as having functional modules that underlie feature extraction. Hence, D2 receptor-enriched and receptor-poor modules may provide a mechanism for functional regulation of compartments within these regions by dopamine.
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PMID:Dopamine D2 receptors are organized in bands in normal human temporal cortex. 886 95

Although several adaptive mechanisms have been identified that mask the existence of Parkinson's disease and delay the onset and aggravation of motor symptoms, the timescale and implications of this compensatory process remain an enigma. In order to examine: (i) the nature of the dopaminergic adaptive mechanisms that come into action; (ii) their sequential activation in relation to the severity of degeneration; and (iii) their efficacy with regard to the maintenance of a normal level of basal ganglia activity, we analysed the brains of mice treated daily with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP, 4 mg/kg, i.p.) and killed at 5-day intervals from day 0 (D0) to D20. Our results demonstrate the sequential activation of two compensatory mechanisms: (i) an increase in striatal tyrosine hydroxylase (TH) protein content attested by the persistence of TH immunolabelling up to D15, contrasting with the decrease observed in both the number of nigral TH-immunoreactive neurons (-70.2%) and striatal dopamine content (-38.4%); (ii) a downregulation of DA uptake in surviving terminals at D20 (73.4% of nigral degeneration). At this point, the failure of adaptive mechanisms to maintain striatal dopaminergic homeostasis is also illustrated by an increase in the cytochrome oxidase activity of substantia nigra pars reticulata, a marker of neuronal function. It has been postulated that an increase in dopamine release per pulse could constitute an adaptive mechanism. The data we present from our MPTP mice model infirm this hypothesis. This study explores the link between the degree of nigral degeneration and the sequential activation of dopaminergic compensatory mechanisms in the nigrostriatal pathway and, in so doing, proposes a rethink of the paradigm applied to these mechanisms.
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PMID:Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse. 1097 32

Exposure to repeated high doses of methamphetamine produces long-term toxicity to central monoamine systems and alters striatonigral pathway function 3 weeks after exposure. To determine whether these changes in the striatonigral pathway persist for longer we examined neuropeptide mRNA expression in the striatum and cytochrome oxidase activity in the output nuclei of the basal ganglia after treatment with multiple high doses of methamphetamine. Rats exposed to multiple high doses of methamphetamine had significant depletion in dopamine and serotonin content, decreases in tyrosine hydroxylase immunoreactivity, and decreases in preprotachykinin mRNA expression, 6 and 12 weeks after methamphetamine treatment. Preprotachykinin mRNA expression was significantly reduced by approximately 20% in the middle striatum and approximately 32% in the caudal striatum, 6 weeks after treatment. Twelve weeks after treatment, preprotachykinin mRNA expression continued to be significantly reduced by approximately 20% in the middle striatum and approximately 14% in the caudal striatum. Cytochrome oxidase histochemical staining in the entopeduncular nucleus and substantia nigra pars reticulata was not significantly different from that in controls at either time point. These data suggest that neurotoxic regimens of methamphetamine induce changes in striatonigral neurons that persist for up to 3 months, although there is some recovery.
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PMID:Long-term post-synaptic consequences of methamphetamine on preprotachykinin mRNA expression. 1235 95

Nitric oxide (NO), in excess, behaves as a cytotoxic substance mediating the pathological processes that cause neurodegeneration. The NO-induced dopaminergic cell loss causing Parkinson's disease (PD) has been postulated to include the following: an inhibition of cytochrome oxidase, ribonucleotide reductase, mitochondrial complexes I, II, and IV in the respiratory chain, superoxide dismutase, glyceraldehyde-3-phosphate dehydrogenase; activation or initiation of DNA strand breakage, poly(ADP-ribose) synthase, lipid peroxidation, and protein oxidation; release of iron; and increased generation of toxic radicals such as hydroxyl radicals and peroxynitrite. NO is formed by the conversion of L-arginine to L-citrulline by NO synthase (NOS). At least three NOS isoforms have been identified by molecular cloning and biochemical studies: a neuronal NOS or type 1 NOS (nNOS), an immunologic NOS or type 2 NOS (iNOS), and an endothelial NOS or type 3 NOS (eNOS). The enzymatic activities of eNOS or nNOS are induced by phosphorylation triggered by Ca(2+) entering cells and binding to calmodulin. In contrast, the regulation of iNOS seems to depend on de novo synthesis of the enzyme in response to a variety of cytokines, such as interferon-gamma and lipopolysaccharide. The evidence that NO is associated with neurotoxic processes underlying PD comes from studies using experimental models of this disease NOS inhibitors can prevent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity. Furthermore, NO fosters dopamine depletion, and the said neurotoxicity is averted by nNOS inhibitors such as 7-nitroindazole working on tyrosine hydroxylase-immunoreactive neurons in substantia nigra pars compacta. Moreover, mutant mice lacking the nNOS gene are more resistant to MPTP neurotoxicity when compared with wild-type littermates. Selegiline, an irreversible inhibitor of monoamine oxidase B, is used in PD as a dopaminergic function-enhancing substance. Selegiline and its metabolite, desmethylselegiline, reduce apoptosis by altering the expression of a number of genes, for instance, superoxide dismutase, Bcl-2, Bcl-xl, NOS, c-Jun, and nicotinamide adenine nucleotide dehydrogenase. The selegiline-induced antiapoptotic activity is associated with prevention of a progressive reduction of mitochondrial membrane potential in preapoptotic neurons. As apoptosis is critical to the progression of neurodegenerative disease, including PD, selegiline or selegiline-like compounds to be discovered in the future may be efficacious in treating PD.
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PMID:Peroxynitrite and mitochondrial dysfunction in the pathogenesis of Parkinson's disease. 1288 Apr 86

We have studied the organization of the hypothalamus in an Australian diprotodontid metatherian mammal, the wallaby ( Macropus eugenii), using cytoarchitectural, histochemical and immunohistochemical techniques. Coronal sections of adult brains were processed for Nissl staining, histochemical reactivity (cytochrome oxidase, nicotinamide adenine dinucleotide phosphate diaphorase and acetylcholinesterase) and immunohistochemistry (antibodies to tyrosine hydroxylase, calbindin, calretinin, non-phosphorylated neurofilament protein, oxytocin and vasopressin). The distribution of immunoreactive neurons for these substances was mapped with the aid of a computer-linked microscope. In general, the wallaby hypothalamus showed a similar nuclear organization to that seen in rodents. The paraventricular nucleus could be divided into several subdivisions based on the different cellular parcellation, similar to that described in rodents. The ventromedial hypothalamic nucleus had cell-sparse dorsomedial and cell-dense ventrolateral subdivisions as seen in eutheria, suggesting a similar functional compartmentalization in all theria. The positions of tyrosine hydroxylase-positive neurons in the wallaby hypothalamus were also similar to those in eutheria. Oxytocin and vasopressinergic neurons were found in all the same major nuclear groups as seen in eutheria, although a nucleus circularis could not be identified. The general similarities between wallaby and eutherian hypothalamus indicate that the basic chemo- and cytoarchitectural features of the hypothalamus are common to eutheria and metatheria and validate the use of the wallaby as a mammalian model of wide applicability in investigations of hypothalamic functional development.
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PMID:Cyto- and chemoarchitecture of the hypothalamus of a wallaby ( Macropus eugenii) with special emphasis on oxytocin and vasopressinergic neurons. 1451 76


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