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

---

Query: EC:1.9.3.1 (cytochrome oxidase)
8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postnatal maturation of cytochrome oxidase and lactate dehydrogenase activity was assessed by histochemistry in rats at 8 postnatal stages, P0, P5, P10, P14, P17, P21, P35 and the adult stage. Enzyme activities were revealed on cryostat brain sections with diaminobenzidine for cytochrome oxidase and nitroblue tetrazolium for lactate dehydrogenase. Lactate dehydrogenase activity remained unchanged between P0 and P10, significantly increased in 8 areas of the 14 studied between P10 and P14 and in 6 structures from P14 to P17. These were mainly parietal, auditory and cerebellar cortices, hippocampus, thalamus, hypothalamus and medial geniculate body. There was no further change until P35 and lactate dehydrogenase activity increased then significantly to reach higher adult levels in hippocampus and medial geniculate body. Cytochrome oxidase activity was low from P0 to P10 and increased in 8 regions between P10 and P14. These were all cortices, caudate nucleus, hippocampus, inferior colliculus and genu. Enzyme activity further increased between P14 and P17 in auditory cortex, medial geniculate body and brainstem, did not vary from P17 to P21 but increased by 92 to 371% in all areas between P21 and P35. Cytochrome oxidase activity rose further from P35 to adult stage in hippocampus and medial geniculate body. From birth to adulthood, cytochrome oxidase activity increased 5 to 19 fold and lactate dehydrogenase activity 1.8 to 3.0. The present study shows that there is a quite good correlation between postnatal changes in regional cerebral glucose utilization and activity of enzymes involved in glycolytic and oxidative glucose metabolism in the rat.
...
PMID:Quantitative histochemical changes in enzymes involved in energy metabolism in the rat brain during postnatal development. I. Cytochrome oxidase and lactate dehydrogenase. 166 81

We examined functional maturation in the mouse whisker-to-barrel pathway from P2 (P0 is the day of birth) to adulthood using the autoradiographic deoxyglucose (DG) method. After intraperitoneal DG injection, left whiskers C1-3 and E1 were stimulated. Sections were cut transversely through the brainstem, and coronally or tangentially through the parietal cortex. After autoradiography, the sections were stained for Nissl or for cytochrome oxidase (CO) activity. In subnuclei caudalis and interpolaris of the spinal trigeminal nucleus ipsilateral to stimulation, DG uptake evoked by the deflection of whiskers C1-3 was present at P2; in subnucleus oralis, nucleus principalis and the contralateral nucleus ventrobasalis of the thalamus, at P4; and in the contralateral barrel cortex, at P7. The first stimulus-dependent DG uptake appeared a few days after the appearance of whisker-related patterns seen in the CO- or Nissl-stained sections. In subnuclei caudalis and interpolaris, areas of stimulus-dependent DG uptake were initially larger than the CO segments representing the stimulated whiskers. Later, areas of stimulus-dependent DG uptake and CO segments matched well. DG uptake evoked by the stimulation of whisker E1 appeared 2-3 days later than that evoked by stimulation of whiskers C1-3. In nucleus principalis, one large area of stimulus-dependent DG uptake covered the representations of the caudal whiskers of all five rows--an observation made at all ages studied. In thalamus, stimulus-dependent DG uptake was found laterally in nucleus ventrobasalis. In barrel cortex, at P7, stimulus-dependent DG uptake was restricted to layers III and IV, but covered more barrels than whiskers stimulated. At P9, a second spot of high DG uptake was seen in deep layer V in register with that in layers III and IV. From P10 onwards, stimulus-dependent DG uptake stretched from layer II to layer VI, and in layer IV, in which it was highest, it was restricted to the barrels C1-3 and E1. In all stations, stimulus-dependent DG uptake decreased in magnitude after P10. While the onset of stimulus-dependent DG uptake is the result of the establishment of functional projections up to that station, the subsequent changes in size of the responding areas may well be due to the partial elimination of terminals, the maturation of local inhibitory circuits, and/or the development of cortical projections to the nuclei of termination and to the thalamic relay.
...
PMID:Maturation of the neuronal metabolic response to vibrissa stimulation in the developing whisker-to-barrel pathway of the mouse. 817 31

The early development of the principal sensory nucleus of the trigeminal nerve (PSN) was examined to determine whether spatiotemporal patterns of synaptogenesis coincide with patterns in neuronal generation, migration, and death. The morphogenesis of PSN neurons during the period from G16 to P14 was studied with a Golgi method. Prenatally, PSN neurons had dendrites that extended into the sensory tract of the trigeminal nerve (s5), and from as early as G18, these dendrites were studded with spines. The dendrites in the s5 degenerated or regressed in the early postnatal period so that the s5 was free of dendrites by P14. The development of anti-synapsin I immunoreactivity was traced from G14 to P10. Immunoreactive puncta (synaptic boutons) appeared in the medial third of the s5 transiently between G18 and P5. On the other hand, puncta in the PSN did not appear until G20, at which time they were confined to the lateral margin of the PSN. By P0, puncta were distributed throughout the PSN. Cytochrome oxidase activity in the PSN was low and unpatterned prenatally. Postnatally, cytochrome oxidase activity intensified and a segmented pattern of barreloids appeared in the ventral PSN on the day of birth. By P5, the complete pattern of barreloids, spanning the full width of the ventral PSN, was evident. The development of cytochrome oxidase activity in the PSN followed the lateral-to-medial gradient of synaptogenesis revealed by the development of synapsin 1 immunoreactivity. This gradient is opposite of that for neuronal generation, migration, and death. Moreover, the s5 serves as a transient synaptic field.
...
PMID:Development of the principal sensory nucleus of the trigeminal nerve of the rat and evidence for a transient synaptic field in the trigeminal sensory tract. 839 50

This study evaluated the effects of neonatal attenuation of axoplasmic transport in the infraorbital nerve (ION) on the organization of vibrissae-related patterns in the rat's CNS. Application of colchicine- or vinblastine- impregnated implants to the ION from birth until postnatal day (P)6 to P10 resulted in a 92.4% reduction in the number of trigeminal (V) ganglion cells labelled by application of horseradish peroxidase to the vibrissa pad and a 44.8% decrease in the number of Nissl-stained ganglion cells in the ophthalamic-maxillary portion of the V ganglion. These implants also decreased the number of myelinated fibres in the ION. In normal rats killed on P6-10, there was an average of 10273 +/- 1259 myelinated axons in the nerve. In the animals with colchicine- or vinblastine-treated implants, this value was 3891 +/- 1965. The highest axon count in an experimental animal was 9859. In all animals, axoplasmic transport attenuation resulted in the disappearance of normal vibrissae-related cytochrome oxidase patterns in the brainstem, thalamus and primary somatosensory cortex. Axoplasmic transport attenuation did not result in the disappearance of vibrissae-related ordering of V primary afferent terminal arbors, as demonstrated by anterograde labelling with neurobiotin. These results suggest that some factor conveyed from the periphery of the V ganglion and perhaps on to the brainstem is necessary for the maintenance of vibrissae-related patterns in the thalamus and cortex.
...
PMID:Effect of neonatal axoplasmic transport attenuation in the infraorbital nerve on vibrissae-related patterns in the rat's brainstem, thalamus and cortex. 892 Dec 52

We followed developmental changes in "barreloid" thalamocortical relay cell (TCR) dendritic arbors between postnatal day 5 (P5; birth = P0) and adulthood. Single neurons in 150- to 250-microns coronal or oblique slices through the somatosensory thalamus in mice of different postnatal ages were injected with lucifer yellow (LY) under direct visualization. Filled cells in the ventroposterior medial nucleus (VPM) were imaged with a confocal microscope, and rendered and analyzed on a computer workstation with special-purpose software. The whisker representation in the thalamus, as revealed by the pattern of barreloids, was demonstrated by oblique illumination of the slices and/or later cytochrome oxidase (CO) staining. VPM cross-sectional area trebles from P5 to adulthood. Barreloids (single-whisker representations) are well delineated in unstained sections until P10-P11; thereafter, barreloids can only be recognized with difficulty with the CO stain. Thalamocortical relay cell (TCR) somal volumes increase rapidly in the first 2 weeks. The number of primary dendrites does not change, nor does the length of the primary dendritic segments, from P5 to adulthood; however, distal dendritic segments elongate and increase in number. Dendritic arbors are confined on P5 to single barreloids; in adults they extend to adjacent barreloids. The postnatal transformation of dendritic arbors by process growth to adjacent barreloids is mainly completed by P18. A change in the developmental role of these cells, from instructing whisker pattern formation to integrating sensory information from more than one whisker, thus occurs after the whisker pattern in the barrel cortex is established. It coincides with the age at which animals are known to begin exploratory whisking behaviors. The mechanism appears to be by growth and remodeling of distal dendrites rather than by oriented growth and regression, as has been reported for stellate cells in cortical whisker barrels.
...
PMID:Postnatal development of mouse "whisker" thalamus: ventroposterior medial nucleus (VPM), barreloids, and their thalamocortical relay neurons. 911 Apr 32

Genetic inactivation of monoamine oxidase A (MAOA) in C3H/HeJ mice causes a complete absence of barrels in the somatosensory cortex, and similar alterations are caused by pharmacological inhibition of MAOA in wild type mice. To determine when and how MAOA inhibition affects the development of the barrel field, the MAOA inhibitor clorgyline was administered to mice of the outbred strain OF1 for various time periods between embryonic day 15 (E15) and postnatal day 7 (P7), and the barrel fields were analyzed with cytochrome oxidase and Nissl stains in P10 and adult mice. High-pressure liquid chromatography measures of brain serotonin (5-HT) showed three- to eightfold increases during the periods of clorgyline administration. Perinatal mortality was increased and weight gain was slowed between P3 and P6. Clorgyline treatments from E15 to P7 or from P0 to P7 disrupted the formation of barrels in the anterior snout representation and in parts of the posteromedial barrel subfield (PMBSF). Treatments from P0 to P4 caused similar although less severe barrel field alterations. Clorgyline treatments only during embryonic life or starting on P4 caused no detectable abnormalities. In cases with barrel field alterations, a rostral-to-caudal gradient of changes was noted: Rostral barrels of the PMBSF were most frequently fused and displayed an increased size tangentially. Thus, MAOA inhibition resulting in increased brain levels of 5-HT affects barrel development during the entire first postnatal week, with a sensitive period between P0 and P4. The rostral-to-caudal gradient of changes in the barrel field parallels known developmental gradients in the sensory periphery and in the maturation thalamocortical afferents. The observed barrel fusions could correspond to a default in the initial segregation of thalamic fibers or to a continued, exuberant growth of these fibers that overrides the tangential domain that is normally devoted to individual whiskers.
...
PMID:Effects of monoamine oxidase A inhibition on barrel formation in the mouse somatosensory cortex: determination of a sensitive developmental period. 954 95

In rodents, the somatosensory cortex has a cell aggregation cluster termed the barrel, reflecting a whisker vibrissa, and this barrel formation is disrupted by infraorbital nerve cut at birth. In the present study, we prepared thalamocortical slice preparations from rats that received infraorbital nerve cut either at birth or at postnatal day (P) 7 and those from normal rats, recorded the optical response reflecting neural excitation in the somatosensory cortex with a voltage-sensitive dye (RH482) and compared the optical responses from lesioned rats with those from normal rats. In normal rats at P10, the optical response elicited electrically by thalamic stimulation propagated to the cortex, and then several patchy clusters appeared in layer IV. The size and location of these patchy responses precisely matched either barrels identified by cytochrome oxidase staining or terminal arbors of thalamocortial axons stained with biotinylated dextran amine. In contrast, at P10 in P0-lesioned rats, clusters having a wider horizontal width but smaller amplitude than those seen in normal rats appeared in layer IV. Correspondingly, neither cytochrome oxidase staining nor biotinylated dextran amine labeling of thalamocortical axons showed any barrel-like clusters or glomerular axon terminals. Likewise, at P5-P6, the tangential width of clusters in layer IV were larger than that in normal rats. At P10 in P7-lesioned rats, small cluster-matched barrels were seen in the optical response as well as in normal rats. These results suggest that P0 infraorbital nerve cut interrupted segregation of functional synapses into the barrels and retarded the maturation of thalamocortical transmission.
...
PMID:Altered spatial patterns of functional thalamocortical connections in the barrel cortex after neonatal infraorbital nerve cut revealed by optical recording. 1036 1

Manipulation of cortical serotonin (5-HT) levels in perinatal rodents produces significant alterations in the development of the layer IV cortical representation of the mystacial vibrissae. Monoamine oxidase A (MAO(A)) knockout mice have highly elevated cortical 5-HT and completely lack barrels in somatosensory cortex (S-I). The present study was undertaken to determine whether the effects on thalamocortical development seen in MAO(A) knockout mice can be replicated in perinatal rats treated with an MAO(A) inhibitor and, second, to determine whether these effects persist with continued treatment or after discontinuation of the drug. Littermates were injected with either clorgyline (5 mg/kg) or sterile saline five times daily. Clorgyline administration from birth to postnatal day (P) 6, 8, or 10 produced increases of 1,589.4 +/- 53.3%, 1660.2 +/- 43.1% and 1,700.5 +/- 84.5 %, respectively, in cortical 5-HT as compared with controls. Serotonin immunocytochemistry, 1,1;-dioctadecyl-3,3,3", 3;-tetramethylindocarbocyanine perchlorate (DiI) labeling of thalamocortical afferents and Nissl and cytochrome oxidase staining of layer IV cellular aggregates demonstrated that clorgyline treatment from P0 to P6 produced a complete absence of any segmentation of vibrissae-related patches in S-I. However, continued treatment until P8 or P10 did not prevent the appearance of these patches. Animals treated with clorgyline from birth to P6 and killed on P8 or P10 had increases of 546.8 +/- 33.2% and 268.8 +/- 6.3% in cortical 5-HT and they had qualitatively normal vibrissae-related patterns in S-I. These results indicate that clorgyline treatment produces a transient disruption of vibrissae-related patterns, despite the continued presence of elevated cortical 5-HT.
...
PMID:Clorgyline treatment elevates cortical serotonin and temporarily disrupts the vibrissae-related pattern in rat somatosensory cortex. 1104 96

In this study, the metabolic activity of rat retinal ganglion cells during postnatal development has been examined in vivo using cytochrome oxidase histochemistry. The intensity of staining was measured by optical densitometry. The activity of cytochrome oxidase in retinal ganglion cells progressively increased from postnatal day 0 (P0) and reached a peak during the second week of postnatal development (P10-P14) and declined thereafter. Our data show that the increased levels of cytochrome oxidase seen in developing retinal ganglion cells occur at the same time, when neuronal maturity and synaptogenesis reach their peaks.
...
PMID:Cytochrome oxidase activity in rat retinal ganglion cells during postnatal development. 1111 18

+/Lc Purkinje cells degenerate postnatally because of a gain-of-function mutation in the delta2 glutamate receptor (Grid2) that causes a constitutive Na+ current leak. The effect of the resulting chronic depolarization on Purkinje cell metabolism was investigated by measuring levels of cytochrome oxidase (COX) activity in Purkinje cell dendrites using quantitative densitometry. Analysis of wild type controls and +/Lc mutants at P10, P15 and P25 showed that levels of COX activity were significantly increased above control levels by P15 and continued to increase through P25. The increase in COX activity is likely to reflect an increase in oxidative phosphorylation to accommodate the energy demands of removing excess Na+ and Ca2+ entering the Purkinje cells in response to the Grid2 leak current.
...
PMID:Cytochrome oxidase activity is increased in +/Lc Purkinje cells destined to die. 1156 33


1 2 Next >>

---