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PubMed1976

Electron paramagnetic resonance spectra of mitochondrial and microsomal cytochrome P-450 from the rat adrenal.

The electron paramagnetic resonance (EPR) spectra of rat adrenal zona fasciculate mitochondria showed peaks corresponding to low spin ferric cytochrome P-450 with apparent g values of 2.424, 2.248 and 1.917, and weak signals due to high spin ferric cytochrome P-450 with gx values of 8.08 and 7.80. The former is attributed to cholesterol side chain cleavage cytochrome P-450, the latter to 11beta-hydroxylase cytochrome P-450. On addition of deoxycorticosterone the g = 7.80 signal was elevated and there was an associated drop in the low spinal signal. As the pH was reduced from 7.4 to 6.1, the g = 8.08 signal increased with again a drop in intensity of the low spin signal. Mitochondria from the zona glomerulosa showed similar spectral properties to those described above. Addition of succinate, isocitrate or pregnenolone caused a loss of the g = 8.08 signal. Addition of calcium increased the magnitude of the g = 8.08 signal, and caused a slight reduction in the magnitude of the low spin signal. Also, addition of deoxycorticosterone, pregnenolone, succinate or isocitrate caused slight shifts of the outer lines of the low spin spectrum. Interaction of mitochondrial cytochrome P-450 with metyrapone and aminoglutethimide modified the low spinal parameters. Adrenal microsomal cytochrome P-450 had low spin ferric g values of 2.417, 2.244 and 1.919 and a high spin ferric gxy values of 7.90 and 3.85, distinct from the values obtained with mitochondria.

Adrenal Glands↗
PubMed1982

Control of phosphatidylinositol turnover in adrenal glomerulosa cells.

The purpose of the present experiments was to compare the effects on phosphatidylinositol metabolism of agents stimulating aldosterone secretion. Glomerulosa cells, isolated from rat adrenals, were incubated in the presence of one of the following stimuli: angiotensin II, elevated potassium concentration, corticotropin, dibutyryl cyclic AMP and prostaglandin E2. Of all these substances, only angiotensin II stimulated the incorporation of [32P]phosphate into phosphatidylinositol. The effect was already detected 2.5 min and was still maintained 60 min after the onset of stimulation. A slight enhancement of the incorporation into other phospholipids was observed in the first minutes of stimulation. Cycloheximide abolished the effect of angiotensin II on aldosterone production, but not on phosphatidylinositol synthesis. In cells prelabelled with [32P]phosphate, radioactivity in phosphatidylinositol relative to that in other phospholipids decreased in response to angiotensin II within 5 min. This indicates that angiotensin II induces a specific breakdown of phosphatidylinositol. Corticotropin failed to enhance the incorporation of [32P]phosphate into phosphatidylinositol and other phospholipids in isolated fasciculate-reticularis cells. The results suggests that although both angiotensin II and potassium are presumed to act through changes in calcium metabolism, angiotensin alone generates the calcium signal by increased phosphatidylinositol turnover.

Adrenal Glands↗
PubMed1989

Neural cell recognition molecule F11: membrane interaction by covalently attached phosphatidylinositol.

The mode of membrane insertion of F11 130 kDa protein, a neural chick cell surface glycoprotein involved in neurite fasciculation, has been investigated. Up to 41% of total F11 130 kDa is released from adult chick brain plasma membranes by phosphatidylinositol specific phospholipase C (PI-PLC), whereas no release is mediated by lecithin/cephalin specific phospholipase C (PLC). PI-PLC dependent release of F11 is also observed from embryonal chick brain plasma membranes and from the surface of intact retinal cells. Biosynthetic labelling experiments demonstrate that F11 contains ethanolamine. Taken together, these results suggest that F11 interacts with the plasma membrane at least partially through covalently linked glycosyl-phosphatidylinositol (GPI) or a structurally similar lipid.

Animals↗
PubMed1991

Purification of recombinant midkine and examination of its biological activities: functional comparison of new heparin binding factors.

Midkine (MK) is the product of a retinoic acid responsive gene, MK, and is the initial member of a new family of heparin binding factors. Recombinant MK produced by an L-cell clone transfected with an MK cDNA was purified to homogeneity. When rat embryonic brain cells were cultured in a serum-free medium on plastic dishes coated with purified MK, a number of neurites extended, formed networks and fasciculated. The majority of neurons continued to extend neurites for a week. In control cultures, neurite extension was observed only in a few cells. Neurotrophic activity of retinoic acid may be mediated by MK. MK had weak but significant mitogenic activity to 3T3 fibroblasts but not to NRK cells. Thus, MK and other members of the family share a part of the activities.

Animals↗
PubMed1992

Functional and morphological changes in cultured neurons of rat cerebral cortex induced by long-term application of aluminum.

Aluminum is an environmental neurotoxin and a suspected risk factor for Alzheimer's disease. The neurotoxicity of aluminum on cultured neurons of rat cerebral cortex was investigated using an assay system for synapse formation and immunohistochemistry. The frequency of spontaneous oscillations of intracellular Ca2+, which is correlated to the number of synapses, was decreased after exposure to 100 microM of aluminum chloride for 22 days. Long-term application of aluminum (48 days) caused aggregation of cell bodies and fasciculation of processes. Processes and cell bodies were strongly stained by antibody to tau protein, which is one of the main components of Alzheimer's neurofibrillary tangles. It is suggested that the characteristics of the degeneration of cultured neurons induced by aluminum show some similarities to the pathology observed in brains with Alzheimer's disease.

Aluminum↗
PubMed1985

Polymorphism among NILE-related glycoproteins from different types of neurons.

We have used biosynthetic, degradative and immunochemical techniques to examine some of the structural features of the NILE (nerve growth factor inducible large external) glycoprotein. Biosynthetic experiments show that the NILE species present on PC12 cells has a core polypeptide with a molecular weight of 160,000 dalton. This polypeptide is initially glycosylated by immature, high mannose oligosaccharides to yield a precursor glycoprotein of 190,000 dalton. Oligosaccharide processing of this precursor in the Golgi apparatus yields the mature 230,000 dalton NILE glycoprotein. NILE-related glycoproteins from different neuronal cell types have molecular weights ranging from 215,000 to 230,000 dalton. Degradative experiments using neuraminidase to remove sialic acid residues and endoglycosidase F to remove all N-linked oligosaccharides indicate that the polymorphism of the NILE-related glycoproteins may be due to differences both at the polypeptide level and at the level of glycosylation. Although NILE glycoproteins and the neural cell adhesion molecule (N-CAM) both appear to be involved in neurite fasciculation, NILE and N-CAM components can be shown to be different from each other by several criteria. (1) The electrophoretic mobilities of NILE and N-CAM are different. NILE-related molecules from various sources migrate as single bands in the range of 215,000-230,000 dalton, while N-CAM from these same sources can exist as 3 separate components of 180,000, 140,000 and 120,000 dalton. (2) Rabbit antibody against NILE does not recognize N-CAM, and rabbit antibody against N-CAM does not recognize NILE. (3) N-CAM is present on some cell types that lack NILE. (4) The core polypeptides of NILE components have apparent molecular weights of about 160,000 dalton, while the N-CAM core polypeptide is about 120,000 dalton in size.

Animals↗
PubMed1987

A group of related surface glycoproteins distinguish sets and subsets of sensory afferents in the leech nervous system.

The distribution of 4 surface glycoproteins on axons of peripheral neurons was studied in the leech Hirudo medicinalis through monoclonal antibodies. All 4 glycoproteins have a similar molecular weight of 130 kDa. Immunohistochemical localization of these glycoproteins on tissue sections of nerves and neuropil reveals tracts of afferent axons organized as nested sets. Their distribution suggests a possible role for these molecules in mediating axon fasciculation.

Animals↗
PubMed1990

Nicotinic actions of oxotremorine on murine skeletal muscle. Evidence against muscarinic modulation of acetylcholine release.

The effects of oxotremorine, arecoline and muscarine on neuromuscular transmission of mouse or rat phrenic nerve-diaphragm were investigated. For some studies of endplate potentials (e.p.p.s) the preparation was immobilized by cutting muscle fibers. Oxotremorine (0.3-10 microM) depolarized endplate membranes, reduced miniature e.p.p. amplitudes but increased frequency, induced spontaneous neural discharges and muscle fasciculations, and produced contracture of denervated mouse diaphragm. In mouse and young rat preparations pretreated with Mn2+, Co2+, Ni2+, Cd2+ or low Ca2+ Tyrode to depress evoked acetylcholine release, oxotremorine 0.3-1 microM increased indirect twitches as well as amplitudes and quantal contents of e.p.p.s. These increases were not observed when the synaptic transmission was not depressed, nor in adult rat preparations. The augmentation by oxotremorine of evoked acetylcholine release persisted in preparations pretreated with neostigmine (1 microM) and tetrodotoxin (20 nM), which inhibited acetylcholinesterase and oxotremorine-induced spontaneous neural discharges. These effects of oxotremorine were mimicked by arecoline but not by muscarine and were antagonized by tubocurarine (0.3 microM) but not by atropine (0.1-10 microM). Atropine alone did not affect indirect twitches, synaptic transmission, tetanic responses evoked by direct stimulation of diaphragms, nor the durations of muscle action potential. The direct twitch responses were only slightly increased by oxotremorine at 2-3 microM. Oxotremorine at high concentrations (greater than 2 microM), depressed indirect twitches and e.p.p. amplitude, and accelerated the run-down of trains of e.p.p.s. The IC50 on indirect twitches was reduced by pretreatment with diltiazem or proadifen, which are known to promote receptor desensitization.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Localization of tyrosine hydroxylase and olfactory marker protein immunoreactivities in the human and macaque olfactory bulb.

These studies utilized specific antisera to examine the distribution and characteristics of tyrosine hydroxylase and olfactory marker protein in the olfactory bulb of the human and macaque monkey. The macaque displayed immunoreactive profiles to both antisera comparable to those described previously for other mammals. Olfactory marker protein antiserum labeled the olfactory nerve layer and glomeruli. Within the glomeruli, labeled processes were interdigitated with unlabeled processes believed to be the postsynaptic dendrites of olfactory bulb neurons. Tyrosine hydroxylase antisera labeled somata surrounding the glomeruli as well as putative dendritic processes with the glomerular neuropil. It appeared that only a subset of juxtaglomerular neurons were immunoreactive. A similar pattern was observed in the human for both antibodies. Fascicles of olfactory marker protein immunoreactive olfactory nerves often coursed long distances into the olfactory bulb prior to arborizing within a glomerulus. The data suggest that olfactory receptor cell axons destined for specific glomeruli fasciculate into bundles prior to reaching the target glomeruli. The immunoreactivity in the human to tyrosine hydroxylase was qualitatively similar to the macaque and other mammals although the number of labeled somata and intraglomerular processes appeared lower. As in the macaque, it appeared that only a subset of juxtaglomerular neurons were labeled.

Adult↗
PubMed1993

Long axon growth from embryonic neurons transplanted into myelinated tracts of the adult rat spinal cord.

Suspensions of embryonic mouse hippocampal neurons were micro-transplanted into the high cervical region of the corticospinal tracts and the ascending dorsal columns of immunosuppressed adult rat hosts. The mouse specific marker, M6, showed that the transplanted neurons grew long, straight, and uniform axons which passed both rostrally and caudally in a narrow beam within the tract occupied by the transplant. The donor axons did not fasciculate with each other, but were intermingled singly with the host myelinated axons, parallel to them and to the host interfascicular glial rows. The donor axons extended at about 0.5 mm per day for the first 6-10 days, after which they slowed down, gradually reaching a maximum distance of around 8 mm from the grafts by 6-7 weeks. Beyond this time M6 ceased to be an effective marker. The presence of the donor axonal projections was confirmed by retrograde cellular labelling of the donor cells from injections of horseradish peroxidase caudal to the transplants in the same host tract. To test whether the donor embryonic hippocampal axons would be attracted to neuropil containing appropriate postsynaptic sites, embryonic rat hippocampal grafts were placed caudal to the mouse grafts. When placed where they could make direct contact with the projection, the rat grafts became M6 positive, suggesting that they had been innervated by mouse axons. But even when placed directly within the beam of donor projections, the rat grafts did not prevent large numbers of mouse axons from continuing caudally in the host spinal tracts. When the rat grafts were placed to one side of the beam of donor projection, the long projecting mouse axons did not deviate from their course. Thus the long ascending and descending myelinated fibre tracts of the adult spinal cord provide a permissive environment for the rapid growth of axons from embryonic donor neurons from a region not normally projecting to the spinal cord. The route taken by these axons is determined by the internal structure of the host tracts. Donor interfascicular axons are able to pass, without deviation, through or beside tissue containing appropriately matched postsynaptic targets.

Animals↗
PubMed1975

Alterations in hepatic drug metabolism and lipid peroxidation during administration of Baygon, a pesticide.

Biochemical studies during low- and high-dose administration of Baygon (a pesticide) to young male rats were performed. It was observed that the activities of drug-metabolizing enzymes were decreased even at a low dose of Baygon and the decrease was much more significant during high-dose injections. Lipid peroxidation was increased with a low dose and the increase was much more pronounced with a high dose. Besides these changes the animals showed physical changes such as salivation, fasciculations, etc. The presence of conjugated diene absorption patterns and malonaldehyde formation indicated the in vivo lipid peroxidation dut to Baygon administration. Toxic effects leading to death were noted when the animals were injected with a high dose of the pesticide, Baygon above 25 mg/kg.

Acetanilides↗
PubMed1983

Embryogenesis of peripheral nerve pathways in grasshopper legs. II. The major nerve routes.

In the preceding paper (H. Keshishian and D. Bentley, 1983a, Dev. Biol. 96, 89-102) the events leading to the morphogenesis of nerve 5B1 in the grasshopper embryonic metathoracic leg were presented. Here the role of later differentiating peripheral neurons in establishing the other major nerves of the leg is examined. In addition to the (tibial 1) (Ti1) pioneer neuron cell pairs that establish nerve 5B1 in the tibia femur, and coxa-trochanter, six later differentiating cells and/or cell pairs were identified and examined with respect to their role in peripheral nerve ontogeny. Nerve path pioneering was observed in two cell pairs of the distal tarsus (Ta1 and Ta2), by neurons of the posterior proximal tibia (Ti2), the posterior midfemur (neurons F3 and F4), and by an additional cell pair in the anterior coxal-trochanteral region of the limb bud (cell pair, CT2). In addition, efferent projections onto limb and epithelia played an important role in establishing nerve branches. In two nerves the axonal trajectory from the periphery to the CNS is established by afferent and efferent pathfinding axons meeting halfway and overgrowing each other's established projections. For each nerve branch examined it was found that axons projected initially to the cell bodies of previously arising neurons along the trajectory. The location along the limb bud ectoderm where neurons arise, and hence their ultimate cell body positions, played an important role in organizing the fasciculation of follower axons and establishing branch points.

Animals↗
PubMed1983

The polarity of axon growth in the wings of Drosophila melanogaster.

We have analyzed the growth of axons in the wings of the mutants Hairy wing and hairy of Drosophila melanogaster. These mutants produce many supernumerary bristle organs and sensilla campaniformia, whose axons grow between the two wing epithelia and can be visualized in both pupal and adult stages. The sensory axons of wild-type animals follow two paths in the wing, within longitudinal veins L1 and L3, and always grow with a distal to proximal polarity. In the mutants, all axons following these two paths likewise grow with correct polarity. Axons elsewhere in the wing, however, are found to grow in many different directions, including from proximal to distal and hence directly away from the central nervous system. A variety of patterns of axon growth and fasciculation are seen in different individuals. Only if the supernumerary axons encounter the two normal paths do they reliably grow toward the base of the wing. We conclude that these two paths provide polarity information for axon growth, information which is either not used or not available elsewhere in the wing in spite of the obvious morphological polarization of every epithelial cell. The time course of neural differentiation suggests that the normal sensory cells of mutant wings, which grow axons relatively early, may be the source of polarity information for the later-differentiating supernumerary cells.

Animals↗
PubMed1986

Altered sensory projections in the chick hind limb following the early removal of motoneurons.

Chick sensory neurons grow to their correct targets in the hindlimb from the outset during normal development and following various experimental manipulations. This may result not because sensory neurons respond to specific limb-derived cues, but because they interact in some way with motoneurons which are responsive to such cues. To test this possibility, we removed the ventral part of the neural tube, which contains motoneurons and their precursors, at stages 16 1/2-20 1/2 and later examined the pathways sensory neurons had taken within the limb. Muscle nerves generally were missing or were reduced in diameter beyond the extent expected simply from the absence of motoneuron axons. In many cases, cutaneous nerves were enlarged, presumably due to the addition of other sensory axons. This result suggests that, in the absence of motoneurons, sensory neurons that normally project to muscles are unable to do so and may instead project along cutaneous pathways. Sensory axons from different segments also crossed less extensively in the plexus region than they did in control embryos, suggesting that alterations in their trajectories may normally be facilitated by similar changes in motoneuron pathways. Thus, motoneurons greatly enhance sensory neuron growth to muscles and contribute significantly toward the achievement of the normal sensory projection pattern. Sensory axons may fasciculate with motoneuron axons, or motoneuron axons may provide an aligned substrate for sensory neurons to grow along. Alternatively, motoneuron axons may alter the environment, thereby making certain pathways in the limb permissive for sensory neuron growth.

Afferent Pathways↗
PubMed1986

Mutant sensory cilia in the nematode Caenorhabditis elegans.

Eight classes of chemosensory neurons in C. elegans fill with fluorescein when living animals are placed in a dye solution. Fluorescein enters the neurons through their exposed sensory cilia. Mutations in 14 genes prevent dye uptake and disrupt chemosensory behaviors. Each of these genes affects the ultrastructure of the chemosensory cilia or their accessory cells. In each case, the cilia are shorter or less exposed than normal, suggesting that dye contact is the principal factor under selection. Ten genes affect many or all of the sensory cilia in the head. The daf-19 (m86) mutation eliminates all cilia, leaving only occasional centrioles in the dendrites. The cilia in che-13 (e1805), osm-1 (p808), osm-5 (p813), and osm-6 (p811) mutants have normal transition zones and severely shortened axonemes. Doublet-microtubules, attached to the membrane by Y links, assemble ectopically proximal to the cilia in these mutants. The amphid cilia in che-11 (e1810) are irregular in diameter and contain dark ground material in the middle of the axonemes. Certain mechanocilia are also affected. The amphid cilia in che-10 (e1809) apparently degenerate, leaving dendrites with bulb-shaped endings filled with dark ground material. The mechanocilia lack striated rootlets. Cilia defects have also been found in che-2, che-3, and daf-10 mutants. The osm-3 (p802) mutation specifically eliminates the distal segment of the amphid cilia. Mutations in three genes affect sensillar support cells. The che-12 (e1812) mutation eliminates matrix material normally secreted by the amphid sheath cell. The che-14 (e1960) mutation disrupts the joining of the amphid sheath and socket cells to form the receptor channel. A similar defect has been observed in daf-6 mutants. Four additional genes affect specific classes of ciliated sensory neurons. The mec-1 and mec-8 (e398) mutations disrupt the fasciculation of the amphid cilia. The cat-6 (e1861) mutation disrupts the tubular bodies of the CEP mechanocilia. A cryophilic thermotaxis mutant, ttx-1 (p767), lacks fingers on the AFD dendrite, suggesting this neuron is thermosensory.

Animals↗
PubMed1988

Morphological differentiation of embryonic rat sympathetic neurons in tissue culture. II. Serum promotes dendritic growth.

In the preceding paper, we reported that embryonic rat sympathetic neurons formed axons, but not dendrites, when they were maintained in the absence of serum and nonneuronal cells. To assess the effects of serum-derived factors on cellular morphology, cultures were initially maintained in serum-free medium while nonneuronal cells were eliminated. Subsequently some cultures were chronically exposed either to fetal calf serum (10%) or to a high-molecular-weight ammonium sulfate fraction of serum (P40 material, 500 micrograms/ml). Phase-contrast microscopy revealed that serum and P40 material did not alter neuronal survival, but did cause flattening of the somata and fasciculation of processes. When neurons exposed to serum or P40 material were injected with Lucifer Yellow, it was found that the majority (greater than or equal to 90%) had local, tapered processes that could be identified as dendrites by light microscopic criteria. These local processes also exhibited other dendritic characteristics in that (1) they reacted with monoclonal antibodies to nonphosphorylated forms of the M and H neurofilament subunits and to microtubule-associated protein 2; and (2) they had substantial amounts of RNA as determined by [3H]uridine autoradiography. Quantitative measurements of the effects of serum and P40 material on dendritic morphology revealed that (1) an 8-day exposure caused most neurons (greater than 80%) to form dendrites; (2) neurons typically had more than one dendrite (mean of 4.1 +/- 0.2 dendrites/cell after a 28-day exposure); and (3) the dendrites were relatively short with the maximum extent of the dendritic arbor being 110 +/- 13 micron after 4 weeks. Serum and P40 material did not routinely cause the formation of supernumerary axons, did not alter radial axonal outgrowth from ganglion explants, and did not significantly increase [3H]leucine incorporation. Thus, serum contains a factor (or factors) which selectively stimulates the extension of dendrites, but not axons. If such a factor were operative in situ, it could play an important role in determining the morphology of sympathetic neurons. In examining the mechanism of serum-induced dendritic growth, we found that even high concentrations (5 micrograms/ml) of nerve growth factor failed to promote dendritic growth in the absence of serum; thus, nerve growth factor by itself is not a sufficient condition for the extension of dendrites.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Distinct roles for adhesion molecules during innervation of embryonic chick muscle.

In vitro studies have suggested that the cell adhesion molecules NCAM and G4/L1 contribute to a variety of events during neural development. We have directly tested the role played by these molecules in the process of initial nerve ingrowth and ramification in the embryonic chick iliofibularis muscle by in ovo injections of specific adhesion-blocking antibodies and analysis of the resultant nerve branching pattern in muscle whole mounts. Antibodies against both molecules produced axonal defasciculation, which resulted in an enhanced transverse projection to the fast region of the muscle. In the case of anti-G4/L1, we also observed a large increase in the number of side branches that form from nerve trunks in the slow region and an enhancement of nerve branching in the fast region. Conversely, anti-NCAM produced a striking decrease in both the number and length of side branches in the slow region, and a reduction in nerve branching in the fast region. A similar reduction of nerve branching was obtained following injection of an endosialidase, which removes sialic acid from NCAM, and which was observed to enhance fiber-fiber apposition, presumably by increasing cell adhesion. Based on their biochemical properties in vitro and their in vivo distribution, both NCAM and G4/L1 are in a position to contribute to axon-axon adhesive interactions, whereas NCAM would be expected to also promote axon-myotube interactions. Our observations in fact indicate that these two adhesion molecules play different but complementary roles during muscle innervation and, specifically, that axon-axon fasciculation is influenced by both NCAM and G4/L1 in an anatomically distinct manner to regulate the overall pattern of nerve branching and that NCAM-mediated axon-myotube interactions are necessary for the attainment of the normal stereotyped pattern of nerve branching in both fast and slow regions of this muscle.

Animals↗