Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines possible changes in energy demands by developing neural crest cells in vitro using cytochrome oxidase (C.O.) histochemistry and immunohistochemical labeling of adrenergic (autonomic) cells and primary sensory neurons. Cytochrome oxidase is a key enzyme for oxidative metabolism and energy production, and it is used as a sensitive metabolic marker for neurons in the brain and dorsal root ganglia. In primary neural crest cell cultures, C.O. staining intensities differ among 4 distinct cellular populations (sensory neurons, adrenergic cells, pigment cells, and non-neuronal neural crest cells). At all stages, pigment cells exhibit extremely low C.O. staining. Neurons (both primary sensory and adrenergic cells) have higher C.O. activity than other cell types such as non-neuronal neural crest cells. This indicates that neurons have higher energy demands and presumably higher levels of functional activity than other cell types at least under the present culture conditions. All neurons in neural crest cell cultures elevate their energy demands during development, implying that energy metabolism and functional activity increase with neuronal maturation. At all stages, early determined sensory neurons exhibit more intense C.O. staining than late-developing sensory neurons. The difference in C.O. activity between the two populations of sensory neurons may be caused by different levels of functional activity due to their different time course of development. Tetrodotoxin (TTX) at 0.5-1 microM concentrations causes a decrease in the level of C.O. activity in the early determined sensory neurons, which may be correlated with a decrease in the functional activity of these neurons. Triple staining combining C.O. histochemistry with indirect immunofluorescence of antibodies against the stage specific embryonic antigen-1 (SSEA-1, which labels quail sensory neurons) and dopamine-beta-hydroxylase (DBH, which labels adrenergic cells) distinguish the level of C.O. activity between sensory neurons and autonomic cells. DBH+ cells exhibit relatively low C.O. staining. However, the C.O. activity among SSEA-1+ neurons varies from high to low levels. In general, SSEA-1+ sensory neurons are much more C.O. reactive than DBH+ autonomic cells. This suggests that developing sensory neurons in culture may have higher spontaneous and/or synaptic activity than autonomic neurons.
 ...
PMID:Developing neural crest cells in culture: correlation of cytochrome oxidase activity with SSEA-1 and dopamine-beta-hydroxylase immunoreactivity. 198 90

The fast axonal transport of [3H]proline-labeled proteins and [3H]fucose-labeled glycoproteins delivered to the dorsal lateral geniculate nucleus in the developing rat optic nerve was investigated during tetrodotoxin-induced monocular impulse blockade. Repeated intraocular injections of various dosages of tetrodotoxin or citrate buffer vehicle were made every two days in rats aged 5-21 days postnatal, and the accumulation of rapidly transported radioactivity in the lateral geniculate nucleus measured between three and twelve hours post-injection at each age. The effectiveness of prolonged tetrodotoxin treatment was monitored by loss of the pupillary light reflex and the level of cytochrome oxidase activity in the contralateral superior colliculus and dorsal lateral geniculate nucleus. Numbers of optic axons proximal to the chiasm and the frequency of retinal ganglion cells per unit distance from the optic disc were examined for signs of tetrodotoxin-induced degeneration of the retinofugal pathway. Tetrodotoxin-treatment reduced the amount of fucosyl glycoproteins, but not proline-labeled proteins, axonally transported to the lateral geniculate nucleus during the first three weeks of postnatal development. Other studies indicated that tetrodotoxin significantly reduced the incorporation of [3H]fucose into retinal proteins indicating that the reduction in transport was probably due to a decrease in precursor incorporation into retinal ganglion cells. Electron microscopy of ganglion cells at 21 days revealed dilated and vacuolated Golgi cisternae associated with tetrodotoxin treatment, suggesting that tetrodotoxin may alter fucose metabolism by secondarily disrupting Golgi organization. Other protein synthetic machinery in these cells, including ribosomes and rough endoplasmic reticulum, appeared normal throughout tetrodotoxin treatment. These data indicate that Na+-dependent optic impulse activity may be indirectly related to the axonal transport of glycoproteins during early postnatal development by mediating the incorporation of precursor into glycoproteins at the Golgi apparatus and their subsequent entrance into the fast transport system.
 ...
PMID:The effect of intraocular injection of tetrodotoxin on fast axonal transport of [3H]proline- and [3H]fucose-labeled materials in the developing rat optic nerve. 241 84

Using immunohistochemical techniques, we demonstrate aspartate aminotransferase (AAT)-like immunoreactivity in cone pedicles and ganglion cells of the cat retina. An identical pattern was seen when we stained for cytochrome oxidase activity, a marker for neurons which have a high metabolic activity. Tetrodotoxin selectively blocked the cytochrome oxidase labeling of ganglion cells. AAT is a key enzyme in the metabolism of aspartate and glutamate and has been proposed as a marker for neurons which use aspartate/glutamate as a neurotransmitter. Due to the close correlation between AAT-like immunoreactivity and cytochrome oxidase activity, we suggest that, at least in the retina, AAT-like immunoreactivity in fact labels cells which have a high metabolic activity.
 ...
PMID:Localization of aspartate aminotransferase and cytochrome oxidase in the cat retina. 298 10